Basic research. Metal ions

Many industries process or use various compounds of mercury, chromium, cadmium, zinc, lead, copper, nickel, arsenic and other substances, which leads to wastewater pollution. To remove these substances from wastewater, currently the most common are reagent treatment methods, the essence of which is to convert water-soluble substances into insoluble ones by adding various reagents and then separating them from water in the form of sediments. The disadvantage of reagent cleaning methods is the irreversible loss of valuable substances with sediment.

Calcium and sodium hydroxides, sodium carbonate, sodium sulfides, various wastes, for example ferrochrome slag, which contains (in%):

Ca – 51.3; MgO – 9.2; SiO2 – 27.4; Cr2O3 – 4.13; Al2O3 – 7.2, FeO2 – 0.73.

The most widely used is calcium hydroxide. Precipitation of metals occurs in the form of hydroxides. The process is carried out at different pH values.

The pH values ​​corresponding to the beginning of precipitation of hydroxides of various metals and complete precipitation (Table 1.10) depend on the nature of the metals, their concentration in solution, temperature, and impurity content. For example, during the joint precipitation of two or more metal ions at pH = const; better results are achieved than when depositing each metal separately. In this case, mixed crystals are formed and adsorption of metal ions occurs on the surface of the solid phase, due to which more complete purification from some metals is achieved.

Table 1.10

pH values ​​during the precipitation of metal hydroxides

* At the initial concentration of the precipitated ion 0.01 mol/l.

** pH values ​​correspond to a residual metal concentration of 10 mol/l.

Purification from mercury compounds. Wastewater contaminated with mercury and its compounds is generated in the production of chlorine and caustic soda, in other electrolysis processes using mercury electrodes, in mercury factories, in some electroplating industries, in the production of dyes, hydrocarbons, and in enterprises using mercury as a catalyst.

Industrial wastewater may contain metallic mercury and its inorganic and organic compounds. Inorganic mercury compounds: oxide - HgO, chloride (mercuric chloride) - HgC12, sulfate - HgSO4, sulfide (cinnabar) - HgS, nitrate - Hg(NO3)2, cyanide - Hg(NCS)2, thiocyanate - Hg(OCN)2, cyanate – Нg(OCN)2. In inorganic compounds, it is mainly Hg2+ ions that are toxic, so the most dangerous are highly soluble and easily dissociating salts.

Organic mercury compounds are used in preserving wood, in the synthesis of organometallic compounds, as pesticides, to protect plastic materials, paper pulp and textiles, and casein adhesives from mold fungi. Organic mercury compounds are very toxic and differ from inorganic salts in that they do not react to Hg ions. In water bodies, mercury, under the influence of organic compounds contained in natural waters, turns into highly toxic compounds. The maximum permissible concentration of mercury in water bodies is 0.005 mg/l.

Metallic mercury can be removed from wastewater through settling or filtration processes. Particles that passed through the filtrate or did not have time to settle are oxidized with chlorine or NaOCl to HgCl2. Then the water is treated with a reducing agent (NaHSO4 or Na2SO3) to remove them and bind the remaining free chlorine. Mercury is precipitated with sodium sulfide, followed by coagulation of the resulting mercury sulfide with ferric chloride. Purification can be carried out with a mixed salt - iron sulfide and barium sulfate.

To separate mercury from wastewater, reduction methods are used: iron sulfide, sodium hydrosulfide, hydrazine, iron powder, hydrogen sulfide gas, etc. Sorption methods for purification from mercury are being widely studied. Ion exchange with vinylpyridine sorbents, the capacity of which reaches 40%, is very effective. The most common way to remove water-soluble mercury compounds is to convert them into poorly soluble mercury sulfide and precipitate it.

The solubility product of HgS in water is 1.6–10–20, which corresponds to a residual concentration in the solution of 2.5–10–21 mg/l. To precipitate Hg, sodium sulfide, sodium hydrosulfide or hydrogen sulfide is first added to wastewater. Then the water is treated with sodium, potassium, magnesium, calcium chlorides or magnesium sulfite in an amount of 0.1 g/l. Under these conditions, mercury sulfide precipitates in the form of granules. To remove fine colloidal particles of mercury sulfide, it is advisable to add coagulants Al(SO4)3∙18H2O, FeSO4∙7H2O, etc.

The mercury sulfide precipitate is separated from wastewater using vacuum filters or filter presses. Separation of HgS to a residual concentration of 0.001 mg/l can also be achieved using carbon filters. Waste coal containing mercury sulfide is burned in a furnace or processed to recover mercury. To remove mercury compounds from solutions, you can also use freshly precipitated iron sulfide, which is obtained by the interaction of S2– or FeSO4∙7H2O, FeCl3∙6H2O ions. For cleaning, a mixture of iron sulfide and barium sulfate can also be used if there is an excess of iron sulfide. Dissolved inorganic mercury compounds can be reduced to metallic mercury and then separated from water.

In addition to precipitation methods, sorption methods can also be used to purify wastewater from inorganic mercury compounds.

The process of formation of mercury amalgam in an electric field has been studied. The method is suitable for treating wastewater containing from 0.01 to 100 mg/l of mercury compounds. In this process, wastewater is filtered through layers of glass balls coated with copper or zinc. The balls are the cathode, and the outer body of the device is the anode. When regenerating the filter load, the polarity of the electrodes is reversed.

Organic mercury compounds are first destroyed by oxidation, such as chlorine gas. After removing excess chlorine, mercury cations are reduced to metallic or converted into sparingly soluble sulfides, followed by removal of the precipitate.

Purification from compounds of zinc, copper, nickel, lead, cadmium, cobalt. Salts of these metals are contained in wastewater from mining and processing factories, metallurgical, machine-building, metal-working, chemical, chemical-pharmaceutical, paint and varnish, textile and other factories.

When treating acidic waters with calcium oxide and sodium hydroxide, the ions of these heavy metals contained in the wastewater are bound into poorly soluble compounds. The composition of salts depends on the pH of the medium. Thus, at pH = 7, zinc hydroxide sulfate of the composition ZnSO4∙3Zn(OH)2 is precipitated, and when the pH increases to 8.8, the composition of the precipitate corresponds to the formula ZnSO4∙5Zn(OH)2. In a highly alkaline environment, the solid phase is mainly hydroxide.

When treating wastewater containing zinc salts with sodium hydroxide, the dosage of the reagent must be carried out with strict control over the pH of the treated wastewater so as not to create conditions for the dissolution of amphoteric hydroxides. The isolation of Zn2+ cations by alkalis is based on their conversion into poorly soluble zinc hydroxide:

The solubility product of zinc hydroxide is 7.1

1018, the beginning of precipitation corresponds to pH = 5.4. At pH = 10.5, the dissolution of amphoteric zinc hydroxides begins, and when pH = 12 is reached, the formation of a complex occurs:

Based on this, cleaning should be carried out at pH = 8-9. Under these conditions, maximum precipitation of zinc hydroxide occurs.

When soda acts on wastewater containing zinc salts, hydroxycarbonates are formed:

At pH values ​​from 7 to 9.5, a basic carbonate of composition is formed; starting from pH = 10, the proportion of hydroxide increases.

Although the precipitation of basic carbonates begins at lower pH values ​​than the corresponding hydroxides, the consumption of soda for precipitation is higher than when using caustic soda or lime. This is explained by the fact that when heavy metals are deposited with soda, the process goes through the stage of formation of hydrocarbonates and an excess of the reagent is required to complete the reaction.

The release of carbon dioxide as a result of precipitation with soda leads to the fact that gas bubbles envelop the sediment particles and lift them, promoting the floating of part of the sediment in settling tanks. The gas must be removed by blowing air once pH = 4.5 is reached.

The disadvantages of caustic soda and soda as reagents also include their relatively high cost and scarcity.

Purification of wastewater from copper involves its precipitation in the form of hydroxide or hydroxide carbonate:

Precipitation of copper hydroxide occurs at pH = 5.3.

The solubility of copper hydroxycarbonate is negligible, so it is most advantageous to precipitate copper in the form of a basic carbonate. To do this, the solution of the neutralizing agent must contain both hydroxide and carbonate ions simultaneously. Consequently, the use of only alkalis or premium lime, which produce hydroxide ions, for the precipitation of copper is impractical. The best reagent for purifying wastewater from copper cations is grade III lime containing “under-burning” (CaCO3).

It is possible to extract copper from wastewater by precipitation with potassium ferrocyanide. This reagent can also be used to precipitate other heavy metal ions.

To remove copper and cadmium from wastewater, a process has been developed by contacting it with sulfur dioxide or sulfites and a powdered metal such as zinc or iron. In this case, the metal reduces sulfites to sulfides, which form sparingly soluble sulfides with heavy metals. At pH = 2 and wastewater temperature of 50 0C, at which the process is carried out, a high degree of purification is achieved.

Treatment of wastewater from nickel is based on its isolation from solution in the form of sparingly soluble compounds:

Precipitation of nickel hydroxide begins at pH=6.7. The solubility product of Ni(OH)2 is 2.0-10–18. As with copper, the concentration of nickel cations is extremely dependent on pH: at pH = 8.0 it is 23.5 mg/l, and at pH = 9.5 only 0.5 mg/l. The solubility product of nickel carbonate is higher than that of hydroxide and is equal to 6.6-10–9. The solubility of nickel hydroxide carbonate is practically zero, therefore, for the most complete removal of nickel, grade III lime containing CaCO3 should be used (as for copper).

Lead cations in solution are precipitated in the form of one of three sparingly soluble compounds:

The beginning of lead hydroxide precipitation corresponds to pH = 6.0. The product of its solubility is 1.1 10–20, that of lead carbonate is 1.0–10–13. Basic lead carbonate is insoluble in water. The data presented shows that all three methods are applicable for lead removal. The cheapest of them is to obtain lead carbonate using limestone, chalk, and marble as a precipitant reagent. Due to the fact that they are hard mineral rocks, they can be used as filter feed through which treated wastewater is filtered.

Despite the fact that wastewater usually contains cations of several metals, it is not possible to use a specific precipitant method to remove each of them. Therefore, wastewater is usually treated with calcium hydroxide (milk of lime), prepared from grade III lime; in this case, simultaneous precipitation of heavy metal cations occurs in the form of hydroxols, hydroxides and carbonates. It has been established that when several metals are deposited together, better results are achieved than when each metal is deposited separately. This is due to the formation of mixed crystals and adsorption of metal ions on the surface of the solid phase.

To increase the degree of purification of wastewater containing heavy metals, it is proposed to introduce a solution into the clarified wastewater in an amount 5-30 times higher than the stoichiometric norm after precipitating their hydroxides with lime at pH 8.5 and separating the sediment. After sludge separation, wastewater with a small content of heavy metal ions can be returned to the circulating water supply system.

Treatment of wastewater with alkaline reagents makes it possible to reduce the content of heavy metals in the solution to values ​​comparable to the maximum permissible concentration for sanitary water bodies. However, when deeper cleaning is required, for example, when directly discharging into fishery reservoirs, cleaning with alkaline reagents does not give the required effect.

Deeper removal of heavy metals is achieved by treating wastewater with sodium sulfide. This is due to the fact that the solubility of heavy metal sulfides is significantly less than the solubility of any other sparingly soluble compounds - hydroxides and carbonates.

To remove small amounts of heavy metal ions, it is possible to use pyrite. The process can be carried out by filtering the wastewater through granular pyrite or by directly introducing the powder into the wastewater. In addition to pyrite, for this purpose you can use the sulfide of any other non-toxic metal, the solubility product of which is greater than the solubility product of the sulfide of the metal extracted from wastewater.

Since hydroxides and sulfides of heavy metals form stable colloidal systems, to intensify the process of their precipitation into wastewater, it is necessary to introduce coagulants and flocculants. Colloidal particles of sulfides have a negative charge, so electrolytes with multicharged cations are used to coagulate sulfides - usually aluminum or ferric sulfates. When coagulating hydroxides, an electrolyte with multicharged anions is required, because colloidal particles are positively charged. Sulfate ions are good coagulants for hydroxides. In addition to electrolyte coagulation, mutual coagulation of colloidal solutions with oppositely charged particles is often used in practice. To speed up the coagulation process, flocculants, mainly polyacrylamide, are used. Adding it in an amount of 0.01% of the dry matter weight increases the rate of precipitation of metal hydroxides by 2-3 times.

The scheme of reagent treatment of wastewater from heavy metal ions with separation of sediments is shown in Fig. 1.59.

The disadvantage of such cleaning is the formation of a large amount of sludge that is difficult to dewater. In addition, purified water contains a large amount of calcium salts, so it is difficult to use in circulating water supply. Based on this, it is proposed to treat the drain after settling sequentially with calcium chloride and soda. In this case, coprecipitation of metal carbonates with calcium carbonate occurs. The resulting crystalline precipitates of metal carbonates have an insignificant volume and are easily dehydrated. At the same time, the water is softened, which makes it possible to use it in a circulating water supply system.

Purification from arsenic compounds. The maximum permissible concentration of arsenic in water bodies is 0.05 mg/l. To purify wastewater from arsenic, reagent, sorption, electrochemical, extraction and other methods are used. The choice of method depends on the form of dissolved arsenic, composition, acidity and other indicators of water.

To purify large volumes of water with a high content of arsenic, the method of chemical precipitation in the form of sparingly soluble compounds (arsenates and arsenites of alkaline earth and heavy metals, arsenic sulfides and trioxide) has found practical application.

Lime milk is widely used to remove oxygen-containing arsenic compounds. At the same time, depending on the composition of wastewater and treatment conditions (pH, temperature, reagent consumption), arsenates and arsenites of various compositions precipitate. The presence of heavy metal ions in wastewater increases the degree of arsenic removal, because Precipitation of arsenates and arsenites of these metals occurs.

Arsenic is precipitated from strongly acidic solutions with sodium sulfide and hydrogen sulfide. Sulfide-alkaline wastewater is purified from arsenic, which is part of the thiosalt anions, using iron sulfate (ferrous sulfate).

Pentavalent arsenic compounds are removed from wastewater better than trivalent arsenic compounds. In addition, storage of sediments containing pentavalent arsenic is cheaper, because it is less toxic and less soluble. Based on this, trivalent arsenic compounds are oxidized to pentavalent arsenic before precipitation. Bleach, chlorine, hypochlorite pulp, hydrogen peroxide, nitric acid, ozone, pyrolusite, etc. are used as oxidizing agents.

Pyrolusite, a natural material consisting mainly of manganese dioxide, is widely used for the oxidation of trivalent arsenic. In an acidic environment the process proceeds as follows:

Optimal oxidation mode: MnO2 consumption is four times compared to stoichiometric, solution acidity is 30-40 g/l sulfuric acid, temperature 70-80 0C, oxidation time 3 hours.

After oxidation of arsenic, it is precipitated in the form of manganese arsenite when neutralized with calcium hydroxide (milk of lime) to pH = 6-9. The sediment is then filtered and buried in waterproof trenches.

Effluents with low concentrations of arsenic are oxidized by filtering water through a layer of pyrolusite. Precipitation is carried out with lime milk in the presence of phosphate ions.

In addition to its oxidizing ability, pyrolusite has sorption properties. The value of its sorption capacity for tri- and pentavalent arsenic is 12.6 and 29.9 mg/l, respectively. As the pH of the solution increases, the amount of arsenic sorbed on pyrolusite and its oxidizing ability decrease. In acidic environments (pH< 1) сорбционная способность падает, а окислительная возрастает.

Other cations and anions present in wastewater, sorbed on pyrolusite, worsen its oxidizing ability.

The oxidizing capacity of manganese dioxide gradually decreases as a result of the processes of sorption and siltation of the surface of pyrolusite grains. To activate, pyrolusite is treated with concentrated sulfuric acid or sodium hydroxide. The acid desorbs arsenic less, but more completely dissolves the sludge formed on the surface of pyrolusite.

Cleaning from iron salts. In natural waters, the iron content ranges from 0.01 to 26 mg/l. In addition, iron is contained in wastewater from chemical, metallurgical, engineering, metalworking, petrochemical, textile, chemical-pharmaceutical and other industries. When the iron content is more than 1 mg/l, the water turns brown. When such water moves through pipelines, iron compounds and iron bacteria are deposited on their walls, reducing the cross-section of the pipeline.

In water bodies, the maximum permissible concentration of iron salts in terms of Fe2+ is 0.5 mg/l. At the same time, in some industries, process water and water in circulation should not contain iron compounds more than 0.05 mg/l, for example in the production of nylon, nylon, cellophane, natural and viscose silk, film, electronics, semiconductors and etc. These industries require deep purification of natural and waste waters from iron compounds.

To deferrize water, aeration, reagent methods, electrodialysis, adsorption, and reverse osmosis are used.

During the aeration process, divalent iron is oxidized into ferric iron. The oxidation reaction in an aqueous solution proceeds according to the following scheme:

Or in total:

In the presence of bicarbonate ions in water, the oxidation of ferrous iron and the hydrolysis of ferric iron proceed according to the reaction:

The oxidation of 1 mg of divalent iron consumes 0.143 mg of oxygen. To ensure a high rate of chemical reaction, the oxygen content in water should be 0.5-0.9 mg per 1 mg of iron.

The aeration process is carried out in a ventilation cooling tower. In the case when it is necessary to enrich water with oxygen and remove part of the free carbon monoxide, cooling towers with chord packing, which are panels made of boards, are used. To roughly estimate the size of a cooling tower, you can proceed from the following: water consumption per 1 m2 of cooling tower area is 40 mg, air consumption is 7 mg of water. Using another attachment is not advisable, because... it may become clogged with iron compounds.

After aeration, it is necessary to separate the iron hydroxide precipitate. For this purpose, sedimentation and filtration processes are used. The iron hydroxide residue can be used to prepare paints or to purify gases from hydrogen sulfide.

During the precipitation of iron hydroxide, the sediment of amphoteric Fe(OH)3 is compacted into hematite Fe2O3: 2Fe(OH)3= Fe2O3 + 3H2O.

If the iron content in water is high, it cannot be completely removed by the aeration method, so reagent methods are used. For this purpose, chlorine, calcium chlorate (bleach), potassium permanganate, ozone, calcium oxide (lime), sodium carbonate (soda), etc. are used. The reagents are dosed into the water before clarifiers or settling tanks.

When interacting with chlorine, the following reaction occurs:

The rate of this reaction increases with increasing pH. The oxidation of 1 mg of divalent iron requires 0.64 mg of Cl;. If calcium chlorate is used, it is used in the form of a 1-2% solution, which is dosed directly into wastewater. The oxidation of ferrous iron with potassium permanganate proceeds according to the equation:

If iron is contained in water in the form of organic compounds or colloidal particles, ozonation is used. In this case, for 1 mass part of iron, 1 mass part of ozone is required.

Purification from manganese compounds. Manganese compounds are found in wastewater from metallurgical, engineering and chemical industries. When the manganese concentration is more than 0.05 mg/l, the water turns dark. Some industries have strict requirements for the manganese content in water (paper, textile, film, copying, synthetic fibers, plastics).

Removing manganese from water can be achieved by the following methods:

1. treating water with potassium permanganate;
2. aeration combined with liming;
3. filtering water through manganese sand or manganese cation exchanger;
4. oxidation with ozone, chlorine or chlorine dioxide.

When treating water with potassium permanganate, simultaneous removal of manganese and iron is achieved. Potassium permanganate is oxidized to form slightly soluble manganese dioxide:

In this process, 1 mg of KMnO4 oxidizes 0.53 mg of Mn +. The greatest effect is achieved when treating water with a dose of 2 mg of KMnO4 per 1 mg. The manganese dioxide precipitate is removed by filtration.

Removal of manganese by aeration with alkalization of water is used with the simultaneous presence of manganese and iron in it. When water is aerated, part of the carbon dioxide is removed and it is saturated with air oxygen. When CO2 is removed, the pH of the wastewater increases, which accelerates the processes of oxidation and hydrolysis of iron and partially manganese with the formation of hydroxides.

Divalent manganese is slowly oxidized into trivalent and tetravalent manganese by oxygen dissolved in water. Manganese oxidation occurs at pH = 9-9.5. The resulting manganese hydroxide precipitates in the form of Mn(OH)3 and Mn(OH)4. The solubility of these compounds is 0.01 mg/l, the resulting Mn(OH)4 again participates in the process, acting as a catalyst for the oxidation of manganese.

At pH = 9.5, manganese is removed almost completely; at pH< 7,5 кислородом воздуха он почти не окисляется. Для ускорения процесса окисления марганца воду после аэрации до подачи на фильтры подщелачивают известью или содой для повышения рН, затем осветляют в осветлителях или отстойниках. Процесс окисления Мn2+ резко ускоряется, если аэрированную воду фильтруют через контактный фильтр, загруженный дробленым пиролюзитом (MnO2∙H2O) либо кварцевым песком, предварительно обработанным оксидами марганца.

Divalent manganese can be removed from water by oxidation with chlorine, ozone or chlorine dioxide. The rate of Mn oxidation by chlorine depends on the pH of the medium. At pH = 7, only 50% of Mn2+ is oxidized in 60-90 minutes. When alkalized with lime to pH = 8, Mn is oxidized almost completely. The consumption of Cl2 for the oxidation of 1 mg of Mn is 1.3 mg. If there are ammonium salts in the water, the consumption of chlorine increases.

Chlorine dioxide and ozone at pH=6.5-7 oxidize Mn2+ in 10-15 minutes. The oxidation of 1 mg of Mn2 requires 1.35 mg of ClO2 or 1.45 mg of O3. However, the use of these oxidizers requires the construction of complex installations, so they are practically not used.

Manganese can be removed from water by biochemical oxidation. The process is carried out as follows. A special type of manganese-consuming bacteria is sown on the filter sand, which absorb manganese from the water during their life processes. Dying bacteria form a porous mass on sand grains with a high content of manganese oxide, which serves as a catalyst for the oxidation process.

Manganese can be removed from water using a manganese cation exchanger, which is prepared by passing solutions of manganese chloride and potassium permanganate through any cation exchanger in sodium form. The following reactions occur:

where Me is the Na+ or K+ cation.

In these processes, potassium permanganate oxidizes manganese to form manganese oxides, which are deposited in the form of a film on the surface of the cation exchanger grains. During regeneration, the film is restored with a solution of potassium permanganate.

Of the methods considered, the most effective is the method of treatment with potassium permanganate. It does not require complex equipment and is easy to control.

Year of issue: 1993

Genre: Toxicology

Format: DjVu

Quality: Scanned Pages

Description: The importance of metal ions for the vital functions of a living organism - for its health and well-being - is becoming more and more obvious. That is why bioinorganic chemistry, rejected for so long as an independent field, is now developing at a rapid pace. Scientific research centers have been organized and are working creatively, engaged in the synthesis, determination of stability and formation constants, structure, reactivity of biologically active metal-containing compounds of both low and high molecular weight. By studying the metabolism and transport of metal ions and their complexes, new models of complex natural structures and the processes occurring with them are designed and tested. And, of course, the main attention is paid to the relationship between the chemistry of metal ions and their vital role.
There is no doubt that we are at the very beginning of the journey. It is with the goal of linking coordination chemistry and biochemistry in the broadest sense of these words that the series “Metal Ions in Biological Systems” was conceived, covering a wide field of bioinorganic chemistry. So, we hope that our series will help break down the barriers between the historically established fields of chemistry, biochemistry, biology, medicine and physics; We expect that a large number of outstanding discoveries will be made in interdisciplinary fields of science.
If the book "Some Questions on the Toxicity of Metal Ions" proves to be a stimulus to new activity in this field, it will serve a good cause, as well as provide satisfaction for the work expended by its authors.

"Some issues of toxicity of metal ions"

G. Sposito. Distribution of potentially hazardous trace metals

1. Potentially hazardous trace metals
2. Metal ion toxicity and atomic structure

Distribution of trace metals in the atmosphere, hydrosphere and lithosphere

1. Atmospheric concentration
2. Concentration in the hydrosphere
3. Concentration in the lithosphere

1. Metal enrichment factors
2. Metal transfer rate

1. Ionic radii
2. Stability series
3. Comparison of stability of metal compounds
4. Metal ion hydrolysis
5. Hard and soft acids and bases
6. pH dependence of stability
7. Preferential metal ion binding sites
8. Ligand exchange rates

Metal Ions Review

1. Alkali metal ions
2. Lithium
3. Magnesium
4. Calcium
5. Barium and strontium
6. Beryllium
7. Lanthanides
8. Aluminum
9. Molybdenum
10. Manganese
11. Iron
12. Cobalt
13. Nickel
14. Cadmium
15. Mercury
16. Thallium
17. Lead

1. Requirements for necessary metals
2. Lack of metals in the natural environment

1. Receipt of metals
2. The role of food and drinking water for metal intake
3. The role of chelating agents secreted by aquatic organisms

1. Mechanism of metal toxicity
2. Sensitivity to essential metals
3. "Functional expressions of toxicity
4. Environmental factors affecting toxicity

1. Tolerance in nature
2. Mechanism of tolerance

1. Laboratory studies of simple power circuits
2. Reactions in a complex semi-natural population
3. Interaction of essential metals with iron

1. Cadmium compounds in soil
2. Availability of cadmium
3. Toxicity of Cd compared to Cu, Ni and Zn
4. Correction of Cd content in soil

1. Copper compounds in soil
2. Availability of copper for plants
3. Symptoms and diagnosis
4. Correction of Cu content in soil

1. Zinc compounds in soil
2. Availability of zinc for plants
3. Symptoms and diagnosis
4. Correction of Zn content in soil

1. Manganese compounds in soil
2. Accessibility for plants
3. Symptoms and diagnosis
4. Correction of manganese content in soil

1. Forms of nickel in soil
2. Accessibility for plants
3. Symptoms and diagnosis
4. Correction of nickel content in soil

1. General aspects
2. Absorption, distribution and excretion of lead in the body
3. Lead toxicity

1. General aspects
2. Absorption, distribution and excretion of arsenic in the body
3. Arsenic toxicity

1. General aspects
2. Absorption, distribution and excretion of vanadium in the body
3. Vanadium toxicity

1. General aspects
2. Absorption, distribution and excretion of mercury in the body
3. Mercury toxicity

1. General aspects
2. Absorption, distribution and excretion of cadmium in the body
3. Cadmium toxicity

1. General aspects
2. Absorption, distribution and excretion of nickel in the body
3. Nickel toxicity

1. General aspects
2. Absorption, distribution and excretion of chromium in the body
3. Chromium toxicity

1. General aspects
2. Absorption, distribution and excretion of uranium in the body
3. Uranium toxicity

1. Necessity, functions, effects of deficiency and needs of the body
2. Absorption, metabolism and excretion in the body
3. Selenium toxicity to animals
4. Selenium toxicity to humans
5. Interactions of selenium with human food components

1. Necessity, function, effects of deficiency, need
2. The effect of excess zinc on the animal body
3. The effect of excess zinc on the human body
4. Interaction of zinc with human food components

1. General characteristics of the peripheral blood lymphocyte system
2. Structural chromosomal abnormalities caused by clastogens
3. Sister chromatid exchange
4. Interference with cytogenetic analysis of lymphocyte culture

1. Arsenic
2. Cadmium
3. Lead
4. Mercury
5. Nickel
6. Other metals

1. Selective phagocytosis of metal-containing particles
2. Uptake of metal ions and the importance of the mechanism of metal entry
3. Localization of carcinogenic metal ions in the nucleus and nucleolus

1. In vitro toxicology
2. Metal ions in in vitro systems

1. Biochemical assessment of metal ion cytotoxicity
2. Biochemical assessment of metal ion genotoxicity

1. Assessment of metal ion cytotoxicity
2. Assessment of the “genotoxicity” of a metal ion

1. Liquid samples
2. Tissue sampling

1. Acid treatment
2. Complexation, extraction and enrichment
3. Mineralization

1. Non-professional sources
2. Professional sources

1. Nickel purification by carbonylation
2. Clinical evaluation of nickel effects and treatment
3. Pathogenesis and mechanism of toxic action

1. Clinical aspects of nickel contact dermatitis
2. Immune mechanism of nickel contact dermatitis
3. Occupational asthma under the influence of nickel

1. Epidemiological data and animal experiments
2. Determining factors and model of nickel carcinogenesis

1. Research objectives
2. Mutagenicity in prokaryotic and eukaryotic systems
3. Mammalian cell culture transformation
4. Chromosomal and DNA abnormalities and associated effects

1. Kidney toxicity
2. Impact on reproduction and development
3. Immunotoxicity
4. Cardiotoxicity

1. Aluminum in the environment
2. On the role of excess aluminum in renal failure

1. Dialysis encephalopathy
2. Dialysis osteodystrophy
3. Suppression of parathyroid function
4. Microcytic anemia

1. Introduction of water treatment
2. Aluminum hydroxide substitutes
3. Searching for other sources

1. Aluminum-containing drugs
2. Dialysate

After studying this chapter, the student should:

know

Basic ecological and physiological data of alkali and alkaline earth metal ions, the effects of lead on the human body, forms of migration of heavy metal atoms in the atmosphere and hydrosphere;

be able to

Determine the suitability of water for various purposes;

own

- methods of protection against anthropogenic impacts of toxic metal ions.

Depending on their behavior in living systems, substances, including metal ions, are divided into five types: necessary for the body; stimulants; inert, harmless; therapeutic agents; toxic. A substance is considered necessary for the body, the deficiency of which causes functional disorders in the body, which can be eliminated by introducing this substance into it. Necessity is an organism-specific property and should be distinguished from stimulation. There are many examples when, as stimulants Both essential and non-essential metal ions appear. Some metals and metal ions at certain concentrations are inert, harmless and do not have any effect on the body. Therefore, inert metals - Ta, Pt, Ag, Au - are often used as surgical implants. Many metal ions can serve therapeutic agents;

In Fig. 6.1 provides an idea of ​​the biological response of body tissues to an increase in the concentration of metal ions supplied in sufficient quantities, for example, from a beggar.

Rice. 6.1. Biological response depending on the concentration required(solid curve)and dangerous(dashed curve)substances

(the relative position of the two curves relative to the concentration scale is arbitrary)

Solid curve indicates an immediate positive response with increasing concentration, starting from zero (it is assumed that the incoming necessary substance saturates its binding sites and does not enter into any other interactions, which in fact are quite possible). This solid curve describes an optimal level covering a wide range of concentrations for many metal ions. The positive effect of increasing metal ion concentrations passes through a maximum and begins to fall to negative values: the body’s biological response becomes negative, and the metal becomes a toxic substance.

Dashed curve in Fig. 6.1 demonstrates the body's biological response to a completely noxious substance that does not exhibit the effects of a necessary or stimulating substance. This curve follows a certain lag, which indicates that a living organism is able to “put up with” small amounts of a toxic substance (threshold concentration) until its toxic effect becomes dominant.

In Fig. 6.1 presents, of course, a certain generalizing picture; Each substance has its own specific curve in “biological response - concentration” coordinates. It also follows from the figure that essential substances can even become toxic if consumed in excess. Almost any substance in excess inevitably becomes dangerous (even if this effect is indirect), for example, due to limited absorption of other necessary substances. The animal body maintains the concentration of substances in the optimal range through a complex of physiological processes called homeostasis. The concentration of all essential metal ions without exception is under strict control of homeostasis; The detailed mechanism of homeostasis for many metal ions remains an area of ​​current research.

The list of metal ions necessary for the human body (and animals) is presented in table. 6.1. As research continues and experimental techniques become more refined, some of the metals previously considered toxic are now considered essential. True, it has not yet been proven that Ni 2+ is necessary for the human body. It is assumed that other metals, such as tin, can also be considered essential for mammals. The second column in the table. 6.1 indicates the form in which a given metal ion exists at pH = 7 and can occur in blood plasma until it combines with other ligands. FeO(OH) and CuO in solid form are not found in plasma, since both Fe 3+ and Cu 2+ form complexes with protein macromolecules. In the third column of the table. Table 6.1 shows the typical total amount of each essential element that is normally present in the adult human body. Accordingly, the metal ion concentrations in plasma are given in the fourth column. And the last column recommends the amount of daily intake for each of the necessary metal ions, but these recommendations are subject to change.

Table 6.1

Essential metal ions

In response to external interference, a living organism has certain detoxification mechanisms that serve to limit or even eliminate the toxic substance. The study of specific detoxification mechanisms in relation to metal ions is at an early stage. Many metals are converted into less harmful forms in the body in the following ways: the formation of insoluble complexes in the intestinal tract; transport of the metal in the blood to other tissues, where it can be immobilized (such as Pb 2+ in bones); conversion by the liver and kidneys to a less toxic or freer form. Thus, in response to the action of toxic ions Cd 2+, Hg 2+, Pb 2+ and others, the human liver and kidneys increase the synthesis of metallothioneins - proteins of low molecular weight, in which approximately 10 (out of 61) amino acid residues are cysteine. The high content and good mutual arrangement of sulfhydryl SH-rpynn provide the possibility of strong binding of metal ions.

The mechanisms by which metal ions become toxic are generally easy to imagine, but difficult to pinpoint for any one specific metal. Metal ions stabilize and activate many proteins; Apparently, for the action of U 3 all enzymes require metal ions. The competition between essential and toxic metal ions for binding sites in proteins is not difficult to imagine. Many protein macromolecules have free sulfhydryl groups that can interact with toxic metal ions such as Cd 2+, Hg 2+, Pb 2+; It is widely believed that this reaction is the pathway for the manifestation of the toxicity of the listed metal ions.

However, it has not been precisely established which protein macromolecules cause the most serious damage to a living organism. Toxic metal ions are distributed among many tissues, and there is no guarantee that the greatest damage occurs where the metal ion is most abundant. This, for example, is shown for Pb 2+ ions: being more than 90% (of their amount in the body) immobilized in the bones, they remain toxic due to the 10% distributed in other tissues of the body. Indeed, the immobilization of Pb 2+ ions in bones can be considered as a detoxification mechanism. This type of toxicity, which is caused by genetic diseases (for example, Cooley's anemia, accompanied by excess iron levels), is not discussed in this chapter.

Our review does not concern the possible carcinogenic activity of metal ions. Captseroheppost - this is a complex phenomenon, depending on the type of animal, organ and level of its development, on synergism with other substances. Metal ions and their complexes can also serve as anticancer agents. The toxicity of a metal ion is usually not related to its need for the body. However, toxicity and necessity have one thing in common: there is generally an interdependence of metal ions with each other, as well as between metal and nonmetal ions, in their overall contribution to their effectiveness. The availability of essential metal ions depends on their interaction with the food consumed; The simple adequacy of the diet does not satisfy this situation. For example, iron from vegetables is poorly absorbed due to the presence of complexing ligands in them, and an excess of Zn 2+ ions can inhibit the absorption of Cu 2+. Similarly, Cd 2+ toxicity is more pronounced in a system with Zn 2+ deficiency, and Pb 2+ toxicity is aggravated by Ca 2+ deficiency. Such antagonism and interdependence greatly complicate attempts to trace and explain the causes of necessity and toxicity.

For many metal ions, acute toxicity occurs when there is a sudden “shock” with a large dose of the metal; in this case, other effects and symptoms appear than with chronic poisoning; Chronic poisoning occurs when receiving low doses of the metal, but over a long period of time.

The most serious toxic effects of metal ions occur through inhalation of dust, typically occurring in industrial settings. Particularly dangerous are particles with a diameter of 0.1 - 1 microns, which are effectively adsorbed by the lungs. Note that the lungs absorb metal ions, which then enter the body fluids, ten times more efficiently than the gastrointestinal tract. For example, the greatest danger from radioactive nlutonium-239 (which emits active alpha particles with a half-life of 24.4 thousand years) comes not from the absorption of plutonium in food, but from the adsorption of plutonium powder by lung tissue.

Volatile metal compounds, such as carbonyl and alkyl compounds of mercury, lead and tin, are readily absorbed by the lungs and can cause acute metal poisoning. Hence the conclusion: any inhalation of metal ions should be avoided!

Alkali metal ions. None of the alkali metals are particularly toxic. Homeostasis maintains the concentration of both essential ions Na + and K + (see Table 6.1) at normal physiological levels. The role of both of these elements is important in digestion. In addition to their specific actions, these metal ions play two critical roles in living organisms: they determine the osmotic balance on both sides of the membrane and provide positive counterions to anions such as HPO, HCO3 and organic molecules, many of which are anions. Thus, the main intercellular and intracellular counterions are Na + and K +, respectively.

Other alkali metal ions can compete with Na + and K + ions in some physiological processes. In the human body, the intracellular fluid, along with K1 ions, contains approximately 0.3 g of Rb +. Small amounts of Cs+ may also be present; a significant amount of 37 Cs (T| 2 = 30 years) appears only in the case of radioactive irradiation. The highest dose of radioactivity of the gonads from internal sources is normally 20 mrem per year and is obtained from natural potassium, which is necessarily present in intracellular fluids.

Lithium. Li* has been used for over 50 years to treat manic-depressive psychosis; In the UK, on ​​average, every two thousand people receive it as a medicine. Oral intake of Li 2 C0 3 raises the concentration of lithium in the blood plasma to 1 mM, which significantly smoothes out changes in the mood of many patients. But the level of metal that is necessary for a therapeutic effect, unfortunately, can have a toxic effect such as inhibition of kidney function and disorders of the central nervous system. The very nature of the action of lithium ions is still not clear; it may alter intracellular interactions. Li+ acts on many enzymes, including those involved in glycolysis. Many biochemists believe that Li + replaces Na b or K + ions, but they are respectively three or six times larger in volume than lithium. Therefore, such a substitution in protein macromolecules should cause a change in the structure of the corresponding metal cavities; on the other hand, the Li + ion is slightly larger than the Mg 2+ ion. Lithium usually forms stronger complexes than Na + and K + , but much weaker than Mg 2+ . In the treatment of psychosis, lithium and magnesium are used in comparable concentrations, and Li + occupies those binding sites that are not occupied by Mg 2+; if all possible places are occupied by magnesium, Li* displaces Na + and K +. All these alkali metal ions enter into exchange reactions more than 10 3 times faster than the Mg 2+ ion. It is this factor that can explain the change in the activity of Mg-containing enzymes upon the introduction of lithium.

Magnesium. This metal in the form of Mg 2+ ion is necessary for both plant and animal organisms. In plants, Mg 2+ is chelated with four nitrogen atoms in the pyrrole rings of the chlorophyll cyclic structure, a rare case of magnesium coordination with nitrogen. In animal organisms, Mg 2+ is a necessary cofactor in every reaction involving adenosine triphosphate (ATP). It also plays the role of a counterion to stabilize the DNA double helix, which has negatively charged phosphate groups in each chain link. The presence of magnesium ions increases the likelihood of correct pairing of links. When coordinated with nucleoside phosphates such as ATP, Mg 2+ binds only to phosphate groups. Mg 2+ ions are absolutely necessary for neuromuscular transmission and muscle contraction. Sustained homeostasis maintains the level of Mg 2+ in the blood plasma at the level of 0.9 mM for practically healthy people. Mg 2+ deficiency is much more common, and in alcoholism it seems to be a mandatory situation. Since severe magnesium deficiency is a rather rare phenomenon, there is little data on the symptoms. Symptoms of this are delirium tremens and neuromuscular manifestations, including chills, convulsions, numbness of the extremities, and tremors. Low levels of Mg 2+ can cause hypocalcemia, in which the metabolically labile mineral cannot be mobilized from the bones. Both Mg 2+ and Ca 2+ levels are controlled by parathyroid hormone through a negative feedback mechanism. Magnesium is quite mildly toxic. Taking large amounts of Mg 2+ salts causes vomiting. Patients with renal failure who received magnesium in acid-neutralizing drugs may experience long-term symptoms of toxicity. The latter can affect the central nervous system, respiratory organs, and cardiovascular system.

Calcium. The two alkaline ions Na~ and K+ and the two alkaline earth ions Mg 2+ and Ca 2+ all together account for more than 99% of the amount of metal ions in the human body. Calcium in the form of Ca 2+ is found in the body more than other metal ions. More than 99% of it is part of bones and tooth enamel in the form of hydroxoapatite Ca 5 (P0 4) 3 (0H). In solution, calcium plays a critical role in many processes, including muscle contraction, blood coagulation, nerve impulses, microtubule formation, intercellular communication, hormonal responses, exocytosis, fertilization, mineralization, as well as cell fusion, adhesion and growth. Many of the listed activities of the calcium ion are involved in interactions with protein macromolecules, which the Ca 2+ ion can stabilize, activate and modulate. All binding sites known so far in proteins for Ca 2+ ions consist of oxygen atoms. The concentration gradient of Ca 2+ in intercellular and intracellular fluids significantly exceeds the gradients of the other three biologically important alkaline and alkaline earth metal ions (Na +, K, Mg 2+). The free concentration of Ca 2+ in intercellular fluids is approximately 1.3 mM, while while in many intracellular fluids it is strikingly low (0.1 μM or even lower for a 20,000-fold concentration gradient). Upon stimulation, the low intracellular concentration can increase 10-fold, which is accompanied by conformational changes in protein macromolecules that have a dissociation constant. within micromoles. The conformational sensitivity of some intracellular proteins to changes in calcium concentration at the micromolar level has led to an understanding of the role of Ca 2+ as an intracellular mediator of the second type. The recommended daily dose (800 mg) of Ca 2+ can be obtained at. drinking a liter of milk - the only calcium-rich source. Calcium deficiency is expressed in growth retardation, bad teeth and other less obvious defects. One such hidden defect is increased absorption of unwanted or toxic metal ions in a Ca 2+ -deficient system. The homeostasis mechanism, which controls absorption from the intestine, controls Ca 2+ levels in humans. Calcium is considered non-toxic. The deposition of bone minerals in soft tissues is not caused by excess Ca 2+ ions, but by increased levels of vitamin D. However, high levels of Ca 2+ in the diet can inhibit the intestinal absorption of other metals needed by the body.

Barium and strontium. Ba 2+ is poisonous due to its antagonism with K + (but not with Ca 2+). This relationship is a clear example of the greater importance of the similarity of the ionic radii of Ba 2+ and K + than the identity of the charge (the two alkaline earth ions Ba 2+ and Ca 2+ have different radii). Barium ion is a muscle poison, treatment here consists of intravenous administration of K + salts. While the Ba 2+ ions are still in the intestine, taking soluble salts SO| _ leads to the formation of insoluble barium sulfate, which is not absorbed. BaSO| used as a radiopaque material for gastrointestinal studies. The human body contains approximately 0.3 g Sr 2+ in bones. This amount does not pose any danger; however, strontium has become extensively contaminated in recent years in the form of 90 Sr (G 1/2 = 28 years) from radioactive fallout.

Beryllium. Be 2+ in acidic environments forms insoluble hydroxide Be(OH) 2, which reduces intestinal absorption. Inhalation of beryllium-containing dust causes chronic pulmonary granulomatosis (called beryllium) or lesions in the lungs; the disease develops slowly and is often fatal. Workers at factories producing fluorescent lamps, where beryllium oxide is used as a phosphorescent substance, have become victims of beryllium disease. (Such production has already been suspended.) A dose of beryllium of one millionth of body weight is already lethal. Be 2+ circulates in the body in the form of colloidal phosphate and is gradually incorporated into the bone skeleton. The formation of hydroxide and phosphate complexes proceeds according to the principles outlined above (in relation to divalent ions of small size, but with a high charge density). Be 2 ~ inhibits many phosphatase-type enzymes and is the strongest known inhibitor of alkaline phosphatase. Beryllium also inhibits enzymes activated by magnesium and potassium and disrupts DNA replication. “Chelation therapy” (taking chelating agents such as ethylenediaminetetraacetic acid) has been shown to be ineffective in removing Be 2+ from the body of people suffering from chronic beryllium poisoning. It is obvious that such a dangerous substance with latent (long-term) toxicity as beryllium should be treated with great caution, and it is better to remove it from circulation altogether.

Lanthanides. The lanthanides include 15 elements, from lanthanum with atomic number 57 to lutetium with atomic number 71. All of them are found in biological systems only in the +3 oxidation state. For gadolinium Gd 3+ - the middle member of this series (atomic number 64) - the ionic radius closely matches the ionic radius of Ca 2+. Because similarity in atomic size is more important than equality of charge, lanthanides replace calcium in many biological systems. This lanthanide substitution is not significant when the metal ion plays a predominantly structural role, but it can have an inhibitory or activating effect when the metal ion is in the active site. Lanthanide ions were used very widely in determining the binding sites of Ca 2+ ions in protein macromolecules. None of the lanthanide elements are biologically essential. Plants resist the accumulation of lanthanides, thereby blocking the transfer of lanthanides to humans mainly through the food chain. Lanthanides are in the form of aqua ion (3+) up to pH = 6, when the formation of hydroxo complexes and sediments begins. Their phosphates are also insoluble. As a result, lanthanides form insoluble complexes in the intestine and are therefore poorly absorbed. None of them are considered toxic.

Aluminum. Being the most abundant metal in the earth's crust, aluminum is rarely found in living organisms, presumably due to the fact that it is difficult to obtain, as it is part of complex mineral deposits. Typically, the adult human body contains 61 mg of aluminum, with the main part in the lungs as a result of inhalation. The only aluminum cation A1 3+ in neutral solutions forms insoluble hydroxide A1(OH) 3 and, on its basis, highly cross-linked hydroxo- and oxo-compounds. It is the formation of such particles and insoluble A1P0 4 that limits the absorption of A1 3+ in the digestive tract. After absorption, the highest concentration of aluminum is in the brain. Deterioration of renal function significantly reduces the body's ability to excrete A1 3+. High levels of aluminum cause phosphate depletion due to the formation of AlP0 4 . Only low levels of this metal are possible in water and food, and at such concentrations A1 3+ is not particularly toxic at all. The entry of Al 3+ (as well as Hg 2+ and Pb 2+) into the water supply network of cities with acid rain leads to a higher metal content, which is already becoming a problem. Metal ions entering waters can pose a danger to fish that is much more serious than acidity. Limited amounts of Ca 2+ and Mg 2+ appear to increase the potential toxicity of aluminum. The toxic effect of A1 3+ manifests itself in the form of constipation and nervous disorders. Increased concentrations of aluminum in the brain are associated with Alzheimer's disease, disorders such as dementia, and even death, mainly in older people. However, according to modern medical concepts, aluminum most likely is not the main cause of the disease, but accumulates in an already unhealthy brain or acts as one of many factors. In any case, the fact that the older generation is using antiperspirants containing aluminum and also ingesting large quantities of antacids (drugs that neutralize acidity) is a very alarming sign. Patients dialyzed with high concentrations of A1 3+ in water may develop “dialysis dementia.”

Chromium. Chromium has traditionally been included in lists of required trace elements. The human body contains about 6 mg of chromium, distributed among many tissues. Although the required doses have not been established, they should be very small. The required level of chromium is difficult to estimate using chemical or biochemical methods. The reason for the need for chromium also remains unknown. Although 25 years have passed since Cr 3+ was first proposed to be a component of glucose tolerance factor, the nature of the complex itself remains unknown and some of the structures proposed for such a complex appear to be unfounded. At pH = 7, the most common compound is Cr(OH)2, but in its inert, polynuclear, complex form. Even in the form of chromium(III) hexaaqua ion, the exchange of a water molecule with a solvent takes several days. It is precisely this inertness that apparently limits the role of Cr(III) to only structural functions. If chromium is nevertheless involved in fast reactions, then it acts in them as Cr (II). Sugars can act as potential ligands for chromium. Glucose is a relatively poor ligand for binding this metal, but this limitation may not play a role in some trivalent chromium complexes. Trivalent Cr(III) is one of the least toxic metal ions; the strong oxidizing agent hexavalent Cr (VI) is already more toxic. At pH

Molybdenum. This metal typically occurs as Mo(VI), and molybdate MoO|“ is adsorbed in the gastrointestinal tract. Molybdenum occurs in plants as a cofactor for the enzyme nitrogenase. Xanthine oxidase (which catalyzes the formation of uric acid in animals) has two Mo atoms, eight Fe atoms and two flavin rings as part of adenine dinucleotide cofactors. Molybdenum toxicity is at the level of copper or sulfur toxicity. In ruminant livestock fed with feed enriched in molybdenum and depleted in copper, tumors occur, which is accompanied by suppressed growth, anemia, and bone diseases. In humans, a diet with a similar ratio of molybdenum to copper causes symptoms of gout. Taking copper preparations is beneficial for animals when they are poisoned with molybdenum. Neither molybdenum nor its related tungsten, which is not essential to the body and inhibits xanthine oxidase activity, are considered particularly toxic metals.

Manganese. Several oxidation states are known for manganese, but there is evidence that this metal does not take part in redox reactions, and only Mn 2+ is important; Mn 3+ is unstable as an aqua ion at pH > 0 and, unless in complex form, is easily reduced to Mn 2+ in neutral solutions. There is no data on what a lack of manganese leads to in the human body. In animals, its deficiency leads to deterioration in bone growth, a decrease in productive function, and possibly suppression of cholesterol synthesis. Manganese can be a cofactor for enzymes. Although many enzymes are activated by Mn 2+, this activation is specific, since other metal ions, such as Mg 2+, are also effective for this purpose. The concentration of Mn 2+ in blood plasma is only one thousandth of the concentration of Mg 2+. Manganese is almost non-toxic, especially in the form of the Mn 2+ ion. The permanganate ion MnOj is toxic due to its oxidizing properties. The most common manganese poisoning occurs due to inhalation of its oxide in industrial production. Chronic action of this kind can lead to manganism, in which serious, irreversible damage to the central nervous system and brain occurs. Apparently, excess manganese in the body has an effect on the enzyme systems of the brain. Unfortunately, there are no universal, effective antidotes; they simply try to eliminate the original cause.

Iron. The iron content in the human body is 4 g, of which about 70%, i.e. 3 g are found in red blood cells in the form of hemoglobin, most of the remainder in iron proteins, and a small amount in some enzymes. Of the recommended daily iron requirement of 10-20 mg, only 10-20% is absorbed, a slightly larger amount in individuals with iron deficiency with good homeostasis. Iron absorption is inhibited by the formation of insoluble hydroxides, phosphates, and complexes with fatty acids; it is promoted by soluble sugar and ascorbic acid chelates. Almost all of the 25 mg of iron released daily by the breakdown of hemoglobin is effectively recycled by the liver, so that the lifespan of iron in the human body exceeds 10 years. That is why absorption of less than 1 mg per day is sufficient for a person (the exception is the period of menstruation, during which a woman loses about 20 mg of iron). The most common human deficiency worldwide is iron deficiency, which affects up to 10% of premenopausal women living in industrial areas; in some groups this figure rises to 100%. Iron deficiency leads to anemia. Iron is absorbed in the form of Fe(II) and is oxidized to Fe(III) in the blood. Since Fe 3+ forms completely insoluble precipitates even in acidic aqueous solutions, the protein transferrin transfers Fe 3+ into the blood. When the Fe 3+-carrying capacity of transferrin is exhausted, Fe(OH) 3 is deposited in the blood. Iron toxicity affects specific groups: in the United States, out of a thousand children, about 10 die annually from swallowing FeS0 4 mineral tablets prepared for mothers; where cooking takes place in iron pots; among alcoholics suffering from severe liver dysfunction. Iron toxicity is associated with gastrointestinal diseases, shock, and liver damage.

Cobalt known as an essential component of vitamin B12, chelated into the complex corrin macrocycle by four linked pyrrole rings. A person's daily requirement for vitamin B 12 is only 3 mcg, and its deficiency results in anemia and stunted growth. Several forms of vitamin B12 are known, which serve as cofactors for enzymes in the methyl group transfer reaction, as well as in other reactions where cobalt undergoes a change in oxidation state. Without being bound in the vitamin B 12 -corrinoid ring, cobalt is found in biological systems in the form of the Co 2+ ion. This ion is capable of binding four, five, and even six donor atoms in various types of coordination polyhedra. Zn 2+ also has a similar ability. These two ions have the same effective ionic radii for all coordination numbers, as well as quite comparable stability constants. In complexes with many ligands, Co 2+ replaces Zn 2+ in some enzymes, often resulting in active enzymes as well. Because it has unpaired ^/- electrons, some spectral methods use Co 2+ to study the properties of spectrally inactive zinc in zinc-containing proteins. Excess Co 2+ stimulates the bone marrow to produce red blood cells; it also reduces the ability of the thyroid gland to accumulate iodine, i.e. Goiter may be a consequence of taking cobalt salts for anemia. Cobalt has shown cardiotoxicity for some avid beer drinkers consuming more than three liters per day. (In some countries, cobalt salts are added to beer at levels of 10 -4% to stabilize the foam to counteract the effects of residual detergents.) Although the number of victims was less than with Co2+ anemia drugs, it is still clear that ethyl alcohol increases the body's sensitivity to cobalt intoxication, and SO 2 contained in bottled beer destroys thiamine (deficiency of this vitamin aggravates cardiotoxicity caused by Co 2+).

Nickel. In biological systems, nickel occurs almost exclusively as Ni(II). Although the +3 oxidation state is possible for nickel under some conditions, it is unlikely to occur in highly evolved organisms. The human body contains about 10 mg of Ni 2+, and the level in the blood plasma is within rather narrow limits, indicating homeostasis and, possibly, the need for nickel. Low levels of Ni2* are stimulating for animals. It serves as a cofactor for the plant enzyme urease. Together with other metal ions, Ni 2 * activates certain enzymes in the body of animals, but its necessity for humans has not yet been proven. The Ni 2+ ion is another example of a metal that is relatively non-toxic. And yet, industrial fumes, especially those involving nickel carbonyl Ni(CO) 4 (in which nickel is formally in a zero-valent state), are easily absorbed in the lungs and are highly toxic. If ingested, Ni 2+ ion causes acute gastrointestinal discomfort. Chronic nickel intoxication leads to the destruction of cardiac and other tissues. The causes of nickel toxicity are unknown to us; it blocks enzymes and reacts with nucleic acids.

Copper. The concentration of copper in the body is regulated by homeostasis, and its optimal concentrations vary widely. That is why neither copper deficiency nor its toxicity are common cases. Copper is an essential cofactor for several enzymes that catalyze a variety of redox reactions. Its deficiency leads to anemia, poor condition of bone and connective tissue, as well as loss of hair pigmentation. It is possible that taking Zn 2+, for example in pills, can cause copper deficiency. Copper in both valence states, Cu(I) and Cu(II), binds well to the sulfhydryl group in glutathione and sulfur-containing proteins. Cu(II) oxidizes the unprotected sulfhydryl group to a disulfide group, self-reducing to Cu(I), so the body must bind Cu(I) before oxidation of the sulfhydryl group occurs. About 95% of copper in blood plasma is found in the protein ceruloplasmin. Although it has one sulfhydryl group, the primary binding site for copper in neutral solutions of plasma albumin is the amino end of the protein molecule, which contains the amine nitrogen, two deprotonated peptide nitrogens, and also the nitrogen of the imidazole ring in the side chain of the third amino acid; all these nitrogen atoms chelate copper, forming a planar cyclic system. Hexaaqua-Cu 2+ becomes more tetragonal (planar) as the number of nitrogen donor atoms increases. A significant amount of copper entering the gastrointestinal tract irritates the nerve endings in the stomach and intestines and causes vomiting. And a chronic excess of copper leads to growth arrest, hemolysis and low hemoglobin content, as well as tissue damage in the liver, kidneys, and brain. There is a deficiency of ceruloplasmin in most patients suffering from Wilson's disease, an inborn defect of metabolism. Such patients exhibit elevated copper levels in the liver along with liver dysfunction. Copper toxicity can be reduced by taking MoO.

Zinc. In humans, the Zn 2+ ion is part of over 20 metal enzymes, including nucleic acids involved in metabolism. Most of the Zn 2+ ions in the blood are found in red blood cells as a necessary cofactor for the enzyme carbonic anhydrase. For zinc, only one oxidation state in solution is known. The role of Zn 2+ in the composition of the enzyme is: a) either in direct binding and polarization of the substrate; b) either indirectly through bound water or hydroxide ion, as in the case of conventional acid-base catalysts and nucleophiles. Most of the Zn 2+ in the human body is found in the muscles, and the highest concentration of zinc is in the gonad - the prostate. The level of Zn 2+ is under homeostasis control. Zinc deficiency is noted in alcoholics, as well as in residents of developing countries whose diet is rich in fibrous and viscous foods. Zinc deficiency is expressed in skin disorders, stunted growth, impaired sexual development and sexual functions in young people. Although aphrodisism is not known in humans, adequate amounts of Zn 2+ are required for normal male sexual behavior. Since human spermatogenesis is a multi-stage process, correcting disorders and restoring sexual health by increasing the concentration of Zn 2+ requires a certain time. Zinc supplementation may unbalance the metabolic equilibrium of other metals, so such interventions should be carried out under strict medical supervision. Let us especially emphasize this advice, since the hypothesis about the Zn 2+ /Cu 2+ ratio as the main causative factor in the development of coronary heart disease (local cessation of arterial blood flow) turned out to be quite correct. Supplementation with divalent zinc promotes wound healing in zinc-deficient patients, but it does not help if adequate amounts of Zn 2+ are present in the body. There is quite a lot of zinc in meat and fish, so supplements are not needed for residents of industrialized countries; Moreover, such additives can be dangerous if given in amounts that interfere with the absorption of copper, iron, and other essential metal ions.

Consumption of excess amounts of zinc salts can lead to acute intestinal disorders accompanied by nausea. Acute poisoning with this element has occurred when consuming sour fruit juices packaged in galvanized (zinc-coated) steel containers. Cases of chronic zinc poisoning in humans are generally unknown, but it may appear blurred and unclear. For example, when zinc and copper compete, an excess of zinc can cause a copper deficiency if the latter is present in minimal quantities. Similarly, excess zinc can retard skeletal development in animals if Ca and P are present in minimal quantities. In general, the zinc ion is not dangerous, and, apparently, the main possibility of poisoning from it is its joint presence with toxic cadmium (in the form of contamination).

Cadmium. Quite rarely, cadmium is present in minerals and soil together with zinc in an amount of approximately 0.1%. Like zinc, this element occurs only as the divalent ion Cc1 2+. The cadmium ion is larger than the zinc ion; it is closer in size to the calcium ion, which allows it to be used as a so-called Ca sample. But still, in terms of its ability to bind ligands, cadmium is more similar to zinc, and therefore, compared to zinc, the number of poisonings was observed in much greater quantities. In contrast to the Ca 2+ ion, both ions of these metals form strong bonds with the donor nitrogen and sulfur atoms of the ligands. Excess cadmium disrupts the metabolism of metals, disrupts the action of zinc and other metal enzymes, which can cause a redistribution of zinc in the body. The exact mechanism of cadmium toxicity is unknown, although it is certainly multi-step.

In complete contrast to the CH 3 Hg + ion, the cadmium ion cannot easily cross the placental barrier, and newborns completely lack this element. In most people, cadmium slowly accumulates from food. The body releases absorbed Cd 2+ very slowly, with a half-life of more than 10 years. The consequence of this is an increase in cadmium content in the kidneys throughout a person's life from zero at birth to approximately 20 mg in old age (for non-smokers) and up to 40 mg for an adult smoker. Most of this element is associated with metallothionein, which are small protein molecules with sulfhydryl substituents, the presence of which in the chain is stimulated by cadmium itself.

Acute cadmium poisoning manifests itself in the form of vomiting, intestinal spasms, and headache; it can even arise from drinking water or other, especially acidic, liquids that have come into contact with Cd-containing compounds in water pipes, cars or cadmium-glazed dishes. Once cadmium enters the body with food, it is transported by the blood to other organs, where it binds to glutathione and hemoglobin of erythrocytes. The blood of smokers contains approximately seven times more cadmium than that of non-smokers. Chronic cadmium poisoning destroys the liver and kidneys and leads to severe renal dysfunction. Unfortunately, there is no specific therapy to treat cadmium poisoning, and chelating agents can only redistribute cadmium to the kidneys (which is also dangerous). Abundant intake of zinc, calcium, phosphates, vitamin D and a high-protein diet can somewhat reduce cadmium poisoning. A particularly serious form of cadmium poisoning has been described in Japan as "itai-itai" disease (the Japanese equivalent of "oh-oh"). The name of the disease comes from the pain in the back and legs that accompanies osteomalacia or bone decalcification (usually in old women), which leads to brittle bones (a known case of 72 fractures in one person). Severe renal dysfunction was also noted due to proteinuria (the appearance of protein in the urine), which continued even after cessation of contact with cadmium. This disease leads to death.

Mercury is toxic in any form. The global release of mercury through gases from the earth's crust and oceans exceeds the amount of mercury produced by humans by at least five times, but its industrial release is more local and concentrated. The average human body contains 13 mg of mercury, which does not provide any benefit. Various mercury salts were used previously as therapeutic agents (for example, mercury benzoate was used to treat syphilis and gonorrhea). The use of mercury reagents as insecticides and fungicides has led to mild and severe poisonings affecting thousands of people. Therefore, mercury poisoning is a worldwide problem.

Mercury can be found in the three most common forms and one less common form, as the mercury ion Hg2+, which is disproportionately divided into elemental mercury and divalent mercury:

For this reaction the value of the equilibrium constant is

indicates that the reaction preferentially proceeds from right to left. But in reality the reaction proceeds from left to right due to the strong complexing ability of the Hg 2+ ion with many ligands. The third common form of mercury is its organic compound methylmercury CH 3 Hg + .

Mercury is a liquid metal at room temperature. Although its boiling point is 357°C, it is highly volatile and therefore more dangerous than is generally believed. One cubic meter of saturated (at 25°C) air contains 20 mg of Hg. This element is almost insoluble in water; solubility limit 0.28 µM at 25°C - 56 µg/l, i.e. 56 parts of mercury to a billion parts of water.

Both mercury cations (Hg 2+ and methylmercury CH 3 Hg +) prefer linear 2-coordination. They form stronger complexes (than most metal ions) with ligands that have a single donor atom, especially N or S. Only mercury, among all the metal ions considered in this chapter, can replace hydrogen in amines (but not in ammonium ions) in alkaline solutions ).

In fact, the word "mercaptan" itself is derived from mercury's strong ability to bind to thiols. In erythrocytes, Hg 2+ ions bind to glutathione and hemoglobin sulfhydryl groups into mixed complexes; Only the proportion of mercury that is usually contained in the human body remains in the blood. Despite the fact that the molecular basis of the toxicity of the Hg 2+ ion is considered to be its interaction with sulfhydryl groups, it remains unknown which proteins undergo metalation.

The rapid exchange of Hg 2+ and CH 3 Hg + in the presence of excess donor ligands such as sulfhydryl groups is of critical importance in toxicology. It is this that determines the rapid distribution of mercury among sulfhydryl residues in tissues. In the blood, the CH 3 Hg' ion is distributed in the same proportion as the SH group is represented: about 10% in plasma and 90% in erythrocytes, which have both hemoglobin and glutathione sulfhydryl groups. To reverse the effects of mercury, BAL (2,3-dimercaptopropanol) is given as an antidote against mercury poisoning; it facilitates the uniform distribution of mercury throughout the body; Hemodialysis with chelating agents such as cysteine ​​or L-acetylpenicillamine is also used.

When inhaled, mercury vapor is actively absorbed and accumulates in the brain, kidneys, and ovaries. Mercury crosses the placental barrier; Acute poisoning causes lung destruction. In the tissues of the body, elemental mercury is converted into an ion, which combines with molecules containing SH groups, including protein macromolecules. Chronic mercury poisoning consists of permanent impairment of the functions of the nervous system, causes fatigue, and at higher levels of poisoning causes the characteristic mercury tremor, when a small trembling is interrupted by noticeable shaking every few minutes. Taking just 1 g of mercury salt is fatal. Mercury salts accumulate in the kidneys, but they are unable, like elemental mercury, to quickly pass the blood or placental barrier. Acute poisoning from ingestion of mercury leads to the precipitation of proteins from the mucomembranes of the gastrointestinal tract, causing pain, vomiting and diarrhea. If the patient survives, the critical organ is the liver. Some hemolysis of red blood cells occurs. Chronic poisoning is expressed in dysfunction of the central nervous system; Lewis Carroll's "Alice in Wonderland" character Mad Hutter is a vivid example of a victim of an occupational disease from poisoning with Hg(N0 3) 2 salt used in fur processing.

Organic mercury derivatives, such as methylmercuric chloride CH 3 HgCI, are highly toxic due to their volatility. Microorganisms in contaminated water containing mercury easily convert inorganic mercury compounds into monomethylmercury CH 3 Hg + . And most of the mercury in the body of fish is in this form, which can persist for years. High levels of CH 3 Hg + are apparently not as toxic for fish as for humans, in whom, when inhaling vapors or ingesting food, CH 3 Hg + ions are actively absorbed and enter the red blood cells, liver and kidneys, and settle in the brain (including in the fetal brain), causing serious cumulative irreversible dysfunction of the central nervous system. In the human body, the half-life of mercury ranges from several months to several years. The toxic effect may be hidden, and symptoms of poisoning may not appear until several years later.

The two most famous examples of mass mercury poisoning were caused by CH 3 Hg + . In 1956, Minamata disease was discovered in southern Japan, near the sea bay of the same name. In 1959, it was shown that this disease is caused by eating fish poisoned by mercury in the form of chloride CH 3 HgCl, discharged by a chemical plant directly into the waters of the bay. The concentration of mercury was so high that the fish died, the birds that ate the fish fell straight into the sea, and the cats that tasted the poisoned food moved “circling and jumping, zigzagging and collapsing.” Already in 1954, such “dances” noticeably reduced the cat population here. But no measurements of mercury pollution in the waters of the bay were made in this area until 1959. And only thanks to the ancient Japanese custom of preserving the dried umbilical cord of their newborns, it became possible to prove that the pollution of the bay with mercury began back in 1947. But until 1968, wastewater was discharged into The bay was not suspended!

For humans, Minamata disease due to methylmercury entering the body began with numbness of the limbs and face, impaired skin sensitivity and motor activity of the hands, for example, when writing. Later, a lack of coordination of movements, weakness, trembling and uncertainty of gait appeared, as well as mental disorders, speech disorders, hearing, and vision. And finally, general paralysis, deformation of the limbs, especially the fingers, difficulty swallowing, convulsions and death. It is also tragic that children born to mothers who were little affected by this disease, who may not have detected its symptoms at all, died from cerebral palsy or became idiots (usually central nervous palsy is not associated with a clear lag in mental development). Apparently, CH 3 Hg + in the mother’s body penetrates the placental barrier into the highly sensitive body of the fetus. Women in more serious stages of the disease became unable to have children.

Thallium. Absorption of extremely toxic thallium compounds by the body leads to gastroenteritis, peripheral neuropathy, and often death. With long-term, chronic exposure to thallium, baldness is observed. The use of TI2SO4 against rodents has been suspended due to its high toxicity to other domestic and wild animals. The main form of thallium in the body is the T1 + ion, although T1C1 is slightly soluble; Thallium also exists in the body in the form of T1 3+. Thallium ions are not much larger than potassium, but they are much more toxic, and the permeability of thallium through cell membranes is the same as that of potassium. Although T1+ and K+ ions are similar in size, the former is almost four times more polarizable and forms strong complexes. For example, it produces insoluble complexes with riboflavin, and therefore can interfere with sulfur metabolism.

Lead has been known for almost five thousand years, and Greek and Arab scientists already knew about its toxicity. The Romans had high levels of lead poisoning because they stored wine and cooked food in lead utensils. Goya, like other artists, suffered from inhalation and accidental exposure to lead paint. Nowadays, high levels of lead pose a danger to urban children due to the fact that they often come into contact with objects painted with lead dyes, play with used batteries, and make crafts from magazine sheets (dyes for color printing contain 0.4% Pb). And most of all, for the reason that they breathe air polluted by car exhausts containing combustion products of tetraethyl lead Pb(C 2 H 5) 4, which is added to gasoline to increase the octane number of the fuel.

The main source of lead contamination is food. Fortunately, the absorption of ingested lead is low due to the formation of insoluble phosphate Pb 3 (P0 4) 2 and basic carbonate Pb 3 (C0 3) 2 (0H) 2. Absorbed lead accumulates in the bones, where it is then released due to osteoporosis, causing delayed toxicity. Today, the average human gel contains about 120 mg of lead, i.e. tens of times more than in Egyptian mummies. In the absence of precipitation-causing ions, at pH = 7, lead is present in the form of the Pb 2+ ion. According to international agreements, the concentration of lead in drinking water should not exceed 50 µg/l. Acute lead poisoning first leads to loss of appetite and vomiting; Chronic poisoning gradually leads to disturbances in kidney function and anemia.

Control questions

• 1. What is the object and subject of research in the bioinorganic chemistry of metal ions?
• 2. List the alkali metal ions (lithium, sodium, potassium, rubidium, cesium). What are their basic ecological and physiological data?
• 3. List the ions of alkaline earth metals (magnesium, calcium, barium, strontium, beryllium, lanthanides). What are their basic ecological and physiological data?
• 4. Explain the effects of lead on the human body. What measures can be proposed to protect human health from lead?
• 5. How do cadmium, mercury, and arsenic enter the human body; what is their impact?
• 6. Why is selenium consumption necessary for a living organism?
• 7. Define bioinorganic chemistry and indicate its place among other environmental sciences.
• 8. Define the concepts “pollutant” and “xenobiotic”. Name typical xenobiotics included in the group of heavy metals.
• 9. 11why do doctors in Moscow and the Moscow region recommend that students and schoolchildren regularly consume foods containing iodine?
• 10. Name the main migration routes of heavy metal atoms in the atmosphere and hydrosphere.
• 11. Characterize various migratory forms from the point of view of the bioavailability of heavy metal atoms.
• 12. Name the main chemical processes that determine the forms of occurrence of heavy metal atoms in the aquatic environment. What is the main difference between the geochemistry of heavy metal atoms in the surface waters of continents and in sea waters?
• 13. How does the presence of humus compounds in water affect the bioavailability of heavy metal atoms? Name the biochemical mechanisms that protect living organisms (plants and animals) from the toxic effects of heavy metal atoms.
• 14. Define heavy metals. What is their role in the biosphere?
• 15. Describe the cycles of chromium and mercury.
• 16. What are the patterns of distribution of chemical elements in the biosphere?
• 17. Name the environmental consequences of industrial pollution of the biosphere.
• 18. Define maximum permissible concentrations (quantities).
• 19. How to determine the suitability of water for various purposes?
• 20. Give the values ​​of the maximum permissible concentrations of pollutants in food products.

Studies of the characteristics of the accumulation of heavy metals by woody plants are associated with the need to assess the biosphere and environment-stabilizing functions of woody plants, which act as a phytofilter on the path of distribution of pollutants in the environment. Woody plants absorb and neutralize some of the atmospheric pollutants, retain dust particles, preserving the surrounding areas from the harmful effects of ecotoxicants.

The interaction of plants with metals that are in the atmosphere and soil, on the one hand, ensures the migration of elements in food chains, despite the fact that these elements are necessary components of plants; on the other hand, there is a redistribution of excesses of some elements, mainly of technogenic origin, in the biosphere. The ability of plants to concentrate part of industrial exhalates in their organs and tissues has been used by humans for many decades.

Features of the redistribution of metals in the “soil-plant” system allow us to conclude that the accumulating ability of woody plants largely depends on the growing conditions and the ability of plants to prevent the penetration of metals into the body

It has been shown that plantations of warty birch and Sukachev larch, in comparison with plantations of Scots pine, have the greatest ability to accumulate technogenic metals.

The accumulation of metals by plants undoubtedly determines their environment-stabilizing and biospheric functions. However, the basics of the resistance and adaptive potential of plants under technogenesis remain largely unexplored. The data obtained on morphophysiological changes in woody plants under technogenic conditions allowed us to conclude that there are no specific plant reactions at various levels of organization - molecular, physiological, cellular and tissue.

The study of the influence of metals on the content of pigments in the leaves of balsam poplar (Populus balsamifera L.) showed that the sum of chlorophylls and carotenoids by the end of the experiment in the test samples decreases (in the case of K+, Ca2+, Mg2+ and Pb2+ ions), increases (Ba2+ and Zn2+ ions ) and does not change (Na+, Mn2+ and Cu2+ ions) compared to the control. When plants are exposed to metal ions, the ratio of pigments changes. It is known that the main photosynthetic pigment of plants is chlorophyll A. With a decrease in the content of chlorophyll A in the leaves, the proportion of auxiliary pigments - chlorophyll B or carotenoids - increases, which can be considered as an adaptive response of the assimilation apparatus of balsam poplar plants to an excess of metal ions in the plant substrate.

It has been established that changes in the ratio of various pigments in the leaves of experimental plants as a result of the action of K+ ions in a long-term experiment are as follows: the proportion of chlorophyll A and carotenoids decreases and the amount of chlorophyll B sharply increases, then a significant decrease in the proportion of chlorophyll B is noted with an increasing amount of carotenoids, by the end of the experiment, the ratio of pigments differs slightly from the control - the proportion of carotenoids increases while the proportion of chlorophylls in the leaves decreases. Na+ and Ca2+ ions generally determine a similar pattern of changes in the ratio of individual pigments, with the exception of the 12th and 24th days of the experiment, when the proportion of chlorophyll B increases significantly relative to chlorophyll A and carotenoids under the influence of Ca2+. The effect of Mg2+ ions is characterized by rather sharp changes in the ratio of individual pigments in the leaves of balsam poplar throughout the experiment. It should be noted that by the end of the experiment, the proportion of chlorophyll A in the leaves of the experimental plants decreased compared to the control.

Under the influence of Ba2+, Zn2+ and Pb2+, abrupt changes in the content of pigments in the leaves of balsam poplar occur. It was shown that during most of the experiment the amount of chlorophyll A in the leaves of experimental plants was lower relative to the control samples. By the end of the experiment, there was a decrease in the proportion of chlorophyll A with an increase in the proportions of chlorophyll B and carotenoids in the leaves of experimental plants relative to control samples.

Mn2+ and Cu2+ ions have an inhibitory effect on the pigment complex of balsam poplar leaves in the first half of the experiment, which is expressed in a decrease in the relative amount of chlorophyll A and an increase in the proportion of minor pigments; in the second half of the experiment, the proportion of chlorophyll A compared to other pigments increases relative to the control (unlike other metals). At the same time, the proportion of chlorophyll B and carotenoids decreases.

Metal ions have different effects on the respiration of balsam poplar (Populus balsamifera L.) leaves. Research in this direction has made it possible to identify several types of responses expressed in changes in leaf respiration: 1) after exposure to metals (up to the 9th day), the respiration of leaves of experimental poplar plants sharply decreases relative to the control, then an increase in respiration is noted (15th day), repeated sharp decrease (24th day) and normalization of respiration by the end of the experiment - for Ba2+, Mg2+ and Pb2+ ions; 2) immediately after treatment of plants, the value of leaf respiration sharply decreases, then an increase is observed, after which a repeated slight decrease and normalization of respiration is noted - for K+ and Cu2+ ions; 3) at first there is an increase, then a sharp decrease, and on the 15th day there is a normalization of the respiration of leaves of experimental plants - for Na+ and Mn2+ ions and 4) metal ions do not have a significant effect on the respiration of leaves, only minor changes in the respiration of experimental plants occur during the experiment for Zn2+ ions.

Based on the nature of changes in the respiration of poplar leaves, Ca2+ can be classified in the first group. However, unlike barium, magnesium and lead, classified in this group, the action of Ca2+ does not normalize the respiration of leaves of experimental plants by the end of the experiment.

The survival of plants under conditions of salt stress, which can be considered an excess content of cations in the environment, is inevitably associated with an increasing expenditure of energy released during respiration. This energy is used to maintain the balance of elements between the plant and the environment. The intensity of respiration and changes in plant respiration can thus serve as integrative indicators of the state of the organism under stress conditions. It has been established that under the influence of K+, Na+, Ba2+, Mg2+, Mn2+, Zn2+, Cu2+ and Pb2+ ions, the respiration of balsam poplar leaves is completely restored within 30 days. Only in the case of Ca2+ is there a 30% decrease in the respiration of leaves of experimental plants.

The discovery of polyvariance in poplar responses to a sharp increase in the concentration of metals in the environment, expressed in changes in respiration and the content of photosynthesis pigments in the leaves, allows us to draw a conclusion about the functioning of a complex of adaptive mechanisms at the molecular physiological level, the work of which is aimed at stabilizing energy costs under stress conditions. It should be noted that complete restoration of respiration occurs both in the case of highly toxic ions (Pb2+ and Cu2+), and in the case of ions of macroelements (Na+ and K+) and microelements (Mg2+ and Mn2+). In addition, the mechanisms of intoxication of highly toxic ions (Pb2+ and Cu2+) are similar to the mechanisms of intoxication of low-toxic ions (Mg2+ and K+).

Metals are an integral part of natural biogeochemical cycles. The redistribution of metals occurs due to the processes of weathering and leaching of rocks, volcanic activity, and natural disasters. As a result of these natural phenomena, natural geochemical anomalies are often formed. In the last century, intensive human economic activity associated with the extraction and processing of minerals has led to the formation of man-made geochemical anomalies.

Over the centuries, woody plants have adapted to changes that naturally occurred in their environment. The formation of an adaptive complex of plants to living conditions is associated with the scale of these changes and the speed of their occurrence. Currently, anthropogenic pressure in intensity and scale often exceeds the influence of extreme natural factors. Against the background of identifying the phenomenon of ecological species specificity of woody plants, establishing the fact of the absence of metal-specific responses in plants has ecological and evolutionary significance, which has become the basis for their successful growth and development under conditions of extreme natural and man-made factors.

The influence of heavy metal ions (Pb2+, Co2+, Zn2+) on the membrane stability of erythrocytes in the blood of a healthy person and various patients was studied. It has been established that heavy metal ions lead to a decrease in the membrane stability of red blood cells. The decrease in erythrocyte persistence depends on the concentration and duration of exposure to metal ions: the higher the concentration and exposure time, the more the erythrocyte density decreases. When examining diseases (acute pneumonia, thyroid tumor, diabetes mellitus), a decrease in the resistance of red blood cells of patients to acid hemolysis is observed. The rate of acid hemolysis decreases in the red blood cells of a patient compared with the red blood cells of a healthy person and depends on the nature of the disease. The data obtained suggest that changes in the physicochemical composition of erythrocytes, manifested by the variability of their resistance, are a consequence of damage to the erythrocyte membrane when exposed to heavy metal ions.

red blood cells

heavy metal ions

1. Bolshoy D.V. Study of the distribution of metals between different blood fractions during exposure to Zn, Cd, Mn and Pb in vitro // Current problems of transport medicine. – 2009. – T.18, No. 4. – pp. 71–75.

2.Gitelzon M.I. Erythrograms as a method of clinical blood testing / M.I. Gitelzon, I.A. Terskov. – Krasnoyarsk: Publishing House of the Siberian Branch of the USSR Academy of Sciences, 1954. – 246 p.

3. Novitsky V.V., Molecular disorders of the erythrocyte membrane in pathologies of various origins are a typical reaction of the body to the contours of the problem / suction // Bulletin of Siberian Medicine. – 2006. – T.5, No. 2. – P. 62–69.

4. Okhrimenko S.M. The influence of tryptophan on some indicators of nitrogen metabolism in animals under oxidative stress caused by cobalt and mercury salts // Bulletin of Dnepropetrovsk University. Biology, Ecology. – 2006. – T.2, No. 4 – P. 134–138.

5.Trusevich M.O. Study of hemolysis of erythrocytes under the influence of heavy metals. Human ecology and environmental problems in the post-Chernobyl period // materials of the republic. scientific conferences. – Minsk, 2009. – P. 50.

6. Tugarev A.A. The influence of cadmium on the morphofunctional characteristics of erythrocytes: abstract. dis. ... dr. biol. Sci. – M., 2003. – 28 p.

7.Davidson T., Ke Q., Costa M. Transport of Toxic Metals by Molecular/Ionic Mimicry of Essential Compounds. – In: Handbook on the toxicology of metals / ed. By G.F. Nordberg et al. – 3-d ed. – Acad. Press. – London/New York/Tokyo, 2007. – pp. 79–84

Recently, much attention has been paid to studying the influence of heavy metal ions on the stability of human red blood cells.

The main target of the toxic effects of heavy metals is the biological membrane.

The erythrocyte is a universal model for studying the processes occurring in the cell membrane under the influence of a wide variety of agents. A detailed study of changes in the morphofunctional parameters of erythrocytes under the influence of various chemical stimuli that a person encounters in the process of natural relationships with nature allows us to more fully establish the possible consequences and determine the most effective ways of their correction under the influence of ecological and chemical environmental factors. The toxic effect of various heavy metal compounds is mainly due to interaction with body proteins, which is why they are called protein poisons. One such metal is cadmium.

A.A. Tugarev proposed a set of informative criteria for assessing the toxic effect of cadmium ions on the morphofunctional parameters of erythrocytes in the peripheral blood of humans and animals.

D.V. The distribution of metals between different blood fractions upon exposure to Zn, Cd, Mn, Pb in vitro has been extensively studied. The author confirmed the literature data on the predominant primary binding of metals in the blood to albumin. According to the penetrating ability, the studied metals were distributed Cd > Mn > Pb > Zn.

The outer membrane of blood cells is rich in functional groups that can bind metal ions.

The biological role of secondary metal binding is very diverse and depends both on the nature of the metal and its concentration and exposure time.

In the works of S.M. Okhrimenko showed an increase in the degree of hemolysis of erythrocytes after the administration of CaCl and HgCl2 salts to animals.

Cobalt ions can directly initiate lipid peroxidation (LPO) and displace iron from heme and hemoproteins, while the mechanism of action of mercury is the binding of SH groups of protein and non-protein thiols. Pre-administered tryptophan partially limits the increase in spontaneous hemolysis of erythrocytes caused by the introduction of cobalt chloride. The absence of such an effect when mercuric chloride is introduced into the body indicates the presence of another mechanism, apparently associated with the high affinity of mercury ions for thio groups of membrane proteins.

M.O. Trusevich studied the effect of heavy metals (chlorides of Co, Mn, Ni, Zn) in final concentrations from 0.008 to 1 mM. Based on the results obtained, the authors concluded that all heavy metals in concentrations above 0.008 mM have a toxic effect on the resistance of the erythrocyte membrane, excluding concentration values ​​of 0.04 mM. For Zn chloride, a decrease in the level of hemolysis of erythrocytes was noted at a concentration of 0.04 mM.

Materials and research methods

In this work, we studied the effect of heavy metals (Pb2+, Co2+, Zn2+) on the membrane stability of erythrocytes in the blood of a healthy person and various patients (diabetes mellitus, thyroid tumor, acute pneumonia).

For the experiments, blood taken from a finger was used. 20 mm3 of blood was collected in 2 ml of physiological solution.

The erythrogram was built according to the method of acid erythrograms proposed by Gitelzon and Terskov.

To monitor the kinetics of hemolysis, a KFK-2 photoelectric colorimeter was used. The standard concentration of erythrocytes was taken, the optical density of which under these conditions was 0.700.

Research results
and their discussion

Solutions of heavy metals (Pb, Co, Zn chlorides) were added to the erythrocyte suspension in final concentrations from 10-5 to 10-3 M. The resulting samples were incubated for 10-60 minutes. Then the optical density of erythrocytes was determined depending on the concentration and time of exposure to heavy metal ions. In addition, the kinetics of acid hemolysis of erythrocytes in the blood of a healthy person and the blood of patients was studied depending on the concentration of heavy metal ions. It is known that the membrane stability of red blood cells changes depending on a person’s age. In this regard, age was taken into account when taking blood.

It has been established that the used heavy metal ions affect the membrane stability of erythrocytes, which is expressed in a change in the density of the latter. Thus, for example, the density of a suspension of erythrocytes exposed to Pb2+ ions at a concentration of 10-3 M for 60 minutes decreases by 90%, and when exposed to Co2+ and Zn2+ ions, by 70 and 60%, respectively (action time 60 minutes, concentration 10-3 M), while the density of the erythrocyte suspension not treated with ions does not change.

Thus, it has been established that the density of the erythrocyte suspension changes depending on the concentration and duration of exposure to heavy metal ions - the higher the concentration and time of exposure, the greater the decrease in erythrocyte density.

From the erythrogram characterizing acid hemolysis of erythrocytes in the blood of a healthy person, it is clear that the onset of hemolysis was at the 2nd minute, the duration of hemolysis was 8 minutes, a maximum of 6 minutes. The rate of acid hemolysis of the blood changes under the influence of heavy metal ions. Thus, if we compare the erythrograms of blood samples that were exposed to Pb2+ ions (concentration 10-3 M, exposure time 30 minutes), we can see that hemolysis lasts on average 4 minutes and the maximum distribution of erythrocytes is 2 minutes; Compared to Pb2+ and Co2+ ions, Zn2+ ions have a weak effect, and acid hemolysis lasts 6.5 minutes, maximum 4 minutes (Fig. 1, 2).

The presented work also studied the kinetics of acid hemolysis of red blood cells in patients with diabetes mellitus, thyroid tumor and acute pneumonia. As can be seen from the data obtained, in the blood of patients with pneumonia and thyroid tumors, there is an accumulation in the group of low-resistant, medium-resistant erythrocytes and a decrease in the number of high-resistant erythrocytes. And in patients with diabetes mellitus, the erythrogram of blood on the right side is elevated. This indicates an increase in the level of erythropoiesis in the blood.

The influence of the heavy metal ions used in the work on the red blood cells of patients is different (Fig. 3, 4, 5). For example, Zn2+ ions have a strong effect on the red blood cells of a patient with acute pneumonia and a thyroid tumor compared to the red blood cells of a healthy person. Our data were confirmed by the results of studies conducted in patients with malignant tumors of various localizations, where pronounced disturbances in protein composition were revealed (a decrease in the content of high-molecular-weight polypeptides while increasing the proportion of low-molecular-weight proteins), and it was also shown that Zn2+ ions are mainly associated with low-molecular-weight proteins. When Pb2+ ions influence the erythrocytes of the blood of patients, a shift of the entire erythrogram to the left is observed, therefore, the entire mass of erythrocytes loses its stability.

Rice. 1. Erythrogram of the blood of a healthy person after exposure to Co2+ ions:
Exposure time 30 min P< 0,5

Rice. 2. Erythrogram of the blood of a healthy person after exposure to Zn2+ ions:
1 - control; 2 - 10-5 M; 3 - 10-4 M; 4 - 10-3 M.
Exposure time 30 min P< 0,5

The data obtained suggest that changes in the physicochemical composition of erythrocytes, manifested in the variability of their resistance, are a consequence of damage to the erythrocyte membrane when exposed to heavy metal ions. The effect of heavy metal ions (Pb2+, Co2+, Zn2+) depends on the concentration, duration of their exposure and the previous state of human health.

Rice. 3. Erythrogram of the blood of patients with pneumonia after exposure to heavy metal ions:
1 - blood of patients with pneumonia; 2 - Co2+ (10-5 M); 3 - Zn2+ (10-5 M); 4 - Pb2+(10-5 M).
Exposure time 30 min P< 0,3

Rice. 4. Erythrogram of blood of patients with a thyroid tumor
after exposure to heavy metal ions:
1 - blood of patients with a thyroid tumor; 2 - Co2+ (10-5 M); 3 - Zn2+ (10-5 M); 4 - Pb2+ (10-5 M). Exposure time 30 min P< 0,4

Rice. 5. Erythrogram of blood of patients with diabetes mellitus after exposure to heavy metal ions:
1 - blood of patients with diabetes; 2 - Zn2+ (10-5 M); 3 - Co2+ (10-4 M); 4 - Pb2+(10-3 M).
Exposure time 30 min P< 0,3

Reviewers:

Khalilov R.I.Kh., Doctor of Physical and Mathematical Sciences, leading researcher at the Laboratory of Radioecology of the Institute of Radiation Problems of the National Academy of Sciences of Azerbaijan, Baku;

Huseynov T.M., Doctor of Biology, Head of the Laboratory of Environmental Biophysics, Institute of Physics of the National Academy of Sciences of Azerbaijan, Baku.

The work was received by the editor on September 17, 2012.

Bibliographic link