Selenium tellurium polonium general characteristics of the elements. Nonmetals of group VI. Oxygen sulfur compounds

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chemical properties

In air, sulfur burns, forming sulfur dioxide - a colorless gas with a pungent odor: S + O2 → SO2 The reducing properties of sulfur are manifested in the reactions of sulfur with other non-metals, but at room temperature sulfur reacts only with fluorine: S + 3F2 → SF6

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Molten sulfur reacts with chlorine, with the possible formation of two lower chlorides 2S + Cl2 → S2Cl2 S + Cl2 → SCl2 When heated, sulfur also reacts with phosphorus, forming a mixture of phosphorus sulfides, among which is the higher sulfide P2S5: 5S + 2P → P2S2 In addition , when heated, sulfur reacts with hydrogen, carbon, silicon: S + H2 → H2S (hydrogen sulfide) C + 2S → CS2 (carbon disulfide)

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Of the complex substances, we should first of all note the reaction of sulfur with molten alkali, in which sulfur disproportions similarly to chlorine: 3S + 6KOH → K2SO3 + 2K2S + 3H2O With concentrated oxidizing acids, sulfur reacts only with prolonged heating: S+ 6HNO3 (conc) → H2SO4 + 6NO2 + 2H2O S+ 2 H2SO4 (conc) → 3SO2 + 2H2O

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At 100–160°C it is oxidized by water: Te+2H2O= TeO2+2H2 When boiled in alkaline solutions, tellurium disproportionates to form telluride and tellurite: 8Te+6KOH=2K2Te+ K2TeO3+3H2O.

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Dilute HNO3 oxidizes Te to telluric acid H2TeO3: 3Te+4HNO3+H2O=3H2TeO3+4NO. Strong oxidizing agents (HClO3, KMnO4) oxidize Te to weak telluric acid H6TeO6: Te+HClO3+3H2O=HCl+H6TeO6. Tellurium compounds (+2) are unstable and prone to disproportionation: 2TeCl2=TeCl4+Te.

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When heated in air, it burns to form colorless crystalline SeO2: Se + O2 = SeO2. Reacts with water when heated: 3Se + 3H2O = 2H2Se + H2SeO3. Selenium reacts when heated with nitric acid to form selenous acid H2SeO3: 3Se + 4HNO3 + H2O = 3H2SeO3 + 4NO.

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When boiled in alkaline solutions, selenium disproportionates: 3Se + 6KOH = K2SeO3 + 2K2Se + 3H2O. If selenium is boiled in an alkaline solution through which air or oxygen is passed, then red-brown solutions containing polyselenides are formed: K2Se + 3Se = K2Se4

ELEMENTS VI A subgroup

(O, S, Se, Te, Po)

General characteristics

Oxygen

Sulfur

Selenium and tellurium

General characteristics of elements

Subgroup VI A of PS includes the elements: oxygen, sulfur, selenium, tellurium and polonium. The common name used for sulfur, selenium, tellurium and polonium is chalcogens. Oxygen, sulfur, selenium and tellurium are non-metals, while polonium is a metal. Polonium is a radioactive element; in nature, it is formed in small quantities during the radioactive decay of radium, so its chemical properties have been poorly studied.

Table 1

Main characteristics of chalcogens

According to the structure of the outer electronic layer, the elements under consideration belong to the p-elements. Of the six electrons in the outer layer, two electrons are unpaired, which determines their valence equal to two. For atoms of sulfur, selenium, tellurium and polonium in an excited state, the number of unpaired electrons can be 4 and 6. That is, these elements can be quadruple or hexavalent. All elements have high electronegativity values, and the EO of oxygen is second only to fluorine. Therefore, in connections they exhibit Art. oxidation -2, -1, 0. The ionization potentials of sulfur, selenium and tellurium atoms are small, and these elements in compounds with halogens have oxidation states +4 and +6. Oxygen has a positive oxidation state in fluorine compounds and in ozone.

Atoms can form molecules with a double bond O 2, ... and connect into chains E - E - ... - E -, which can exist in both simple and complex substances. In terms of chemical activity and oxidizing ability, chalcogens are inferior to halogens. This is indicated by the fact that in nature oxygen and sulfur exist not only in a bound state, but also in a free state. The lower activity of chalcogens is largely due to stronger bonds in the molecules. In general, chalcogens are very reactive substances, the activity of which increases sharply with increasing temperature. Allotropic modifications are known for all substances of this subgroup. Sulfur and oxygen practically do not conduct electric current (dielectrics), selenium and tellurium are semiconductors.

When moving from oxygen to tellurium, the tendency of elements to form double bonds with small atoms (C, N, O) decreases. The inability of large atoms to form π bonds with oxygen is especially evident in the case of tellurium. Thus, tellurium does not have acid molecules H 2 TeO 3 and H 2 TeO 4 (meta-forms), as well as TeO 2 molecules. Tellurium dioxide exists only in the form of a polymer, where all the oxygen atoms are bridging: Te – O – Te. Telluric acid, unlike sulfuric and selenic acid, occurs only in the ortho form - H 6 TeO 6, where, as in TeO 2, Te atoms are connected to O atoms only by σ bonds.

The chemical properties of oxygen differ from the properties of sulfur, selenium and tellurium. On the contrary, the properties of sulfur, selenium and tellurium have many similarities. When moving through the group from top to bottom, one should note an increase in acidic and reducing properties in the series of compounds with hydrogen H 2 E; an increase in oxidative properties in a number of similar compounds (H 2 EO 4, EO 2); decrease in thermal stability of chalcogen hydrogens and salts of oxygen acids.

The oxygen subgroup includes five elements: oxygen, sulfur, selenium, tellurium and polonium (a radioactive metal). These are p-elements of group VI of D.I. Mendeleev’s periodic system. They have a group name - chalcogens, which means “ore-forming”.

Properties of oxygen subgroup elements

Chalcogen atoms have the same structure of the external energy level - ns 2 nр 4 . This explains the similarity of their chemical properties. All chalcogens in compounds with hydrogen and metals exhibit an oxidation state of -2, and in compounds with oxygen and other active non-metals - usually +4 and +6. For oxygen, as for fluorine, the oxidation state equal to the group number is not typical. It exhibits an oxidation state of usually -2 and in combination with fluorine +2. Such values ​​of oxidation states follow from the electronic structure of chalcogens

The oxygen atom in the 2p sublevel has two unpaired electrons. Its electrons cannot be separated because there is no d-sublevel on the outer (second) level, i.e. there are no free orbitals. Therefore, the valence of oxygen is always equal to two, and the oxidation state is -2 and +2 (for example, in H 2 O and ОF 2). The same are the valence and oxidation states of a volume of sulfur in an unexcited state. When transitioning to an excited state (which occurs when energy is supplied, for example, during heating), the sulfur atoms are first separated r- , and then 3s electrons (shown by arrows). The number of unpaired electrons, and, consequently, the valence in the first case is four (for example, in SO 2), and in the second - six (for example, in SO 3). Obviously, even valencies 2, 4, 6 are characteristic of sulfur analogues - selenium, tellurium and polonium, and their oxidation states can be equal to -2, +2, +4 and +6.

Hydrogen compounds of elements of the oxygen subgroup correspond to formula H 2 R (R - element symbol): H 2 O, H 2 S, H 2 S e, N 2 Te. They calledthere are chalconhydrogens. When dissolved in water they formacids. The strength of these acids increases with increasing serial number of the element, which is explained by the decrease in energy bonds in the series of compounds H 2 R . Water dissociating into H+ and O ions N - , is amphoteric electrolyte.

Sulfur, Selenium and tellurium form the same forms of compounds with oxygen type R O 2 and R O 3- . They correspond to acids of type H 2 R O 3 and H 2 R O 4- . As the atomic number of an element increases, the strength of these acids decreaseswat. All of them exhibit oxidizing properties, and acids like H 2 R O 3 are also restorative.

The properties of simple substances change naturally: with increasingcharge of the nucleus, non-metallic ones weaken and metallic ones increase properties. Thus, oxygen and tellurium are non-metals, but the latter hasmetallic luster and conducts electricity.

Selenium is an essential trace element for humans and animals. It is one of the biologically important trace elements present in the human body and involved in the metabolic, biophysical and energetic reactions of the body, ensuring the viability and function of cells, tissues, organs and the body as a whole. The role of selenium is especially important for the functional activity of organs such as the heart, liver, kidneys, etc.
Selenium is an element of group 4 of the main subgroup of the periodic table of Mendeleev, largely repeating the chemical properties of sulfur. Selenium is able to replace sulfur in sulfur-containing amino acids with the formation of selenoamino acids, which are more active biologically and are stronger protectors of ionizing radiation than sulfur-containing amino acids. In addition, selenoamino acids help reduce the amount of free radicals that disrupt the activity and properties of enzymes and amino acids.
Selenium enters the human body from the soil with crop and livestock products, which determines the dependence of the level of microelement supply on geochemical living conditions.
However, not all soil selenium is available to plants. Thus, in acidic, heavily waterlogged soils, the bioavailability of the microelement is low, although the total content can be significant.
Taking into account that the optimal level of selenium intake, corresponding to the maximum activity of glutathione peroxidase (GPX) of platelets or the selenium content in the blood serum of 115-120 μg/l, is 120 μg/day, the established selenium concentrations correspond to a moderate supply of the population with the microelement in most of the studied territories, Moreover, in none of the regions have cases of severe selenium deficiency been registered - the content in the blood serum is less than 50 μg/l. In Russia, average serum selenium concentrations range from 62 µg/L in the west to 145 µg/L in the east.
In plants, the most important chemical form of selenium is selenomethionine. Most selenium in animal tissues is present in the form of selenomethionine and selenocysteine.
The biochemical functions of selenium are determined by selenium-containing proteins (SP). A lack of microelement can lead to disruption of cellular integrity, changes in the metabolism of thyroid hormones, the activity of biotransforming enzymes, increased toxic effects of heavy metals, and increased concentrations of glutathione in plasma.
A characteristic feature of mammalian SBs is that they appear to be associated with redox processes occurring inside and outside the cell. To date, 12 SBs containing selenium in the active site have been characterized.
- GPX1 (cCPX) – cellular glutathione peroxidase – it is assumed to be present in all cells of the mammalian body, apparently used as a selenium depot, an antioxidant.
- GPX2 (CPX-CI) – localized in gastric epithelial cells
- GPX3 (pCPX) – intercellular GPX or plasma GPX, controls the level of peroxides outside the cell, the function of the enzyme is not clear, however, it has been shown that the activity of pCPX is restored faster than cCPX, which may indicate the greater importance of this enzyme.
- GPX4 (PHCPX) is a phospholipid, localized mainly in the testes, but found in membranes and cytosol. Restores hydroperoxides of cholesterol, its esters, phospholipids, plays an important role in the male reproductive system.
- ID – group 3 oxidoreductases, regulate the activity of thyroxine. Animal experiments have shown that simultaneous deficiency of selenium and iodine leads to more severe hypothyroidism than deficiency of iodine alone. Some authors suggest that cretinism in newborns may be a consequence of a combined deficiency of these 2 elements in the mother.
- ID1 is an enzyme involved in the metabolism of thyroxine and triiodothyronine. This microsomal enzyme is localized in the liver, kidneys, thyroid gland and central nervous system.
- ID2 – catalyzes the conversion of thyroxine to triiodothyronine
- ID3 – deactivates thyroxine and triiodothyronine, localized in the central nervous system, skin, placenta. Participates in energy metabolism.
- Mammalian TR – main function – catalyzes NADPH-dependent reduction in the cytosol.
- SPS2 is an enzyme that catalyzes the ATP-dependent activation of selenium to form selenophosphate.
- SelP is a glycoprotein that can act as an antioxidant and selenium depot. It is quickly synthesized with the introduction of selenium supplements. Participates in the decontamination of heavy metals.
- Selenoprotein W (SelW) is an intercellular protein present in many tissues, mainly in muscles and brain. It is assumed to participate in redox reactions and influence the development of cancer.
Data from isotopic analysis and the results of theoretical studies suggest that there may be from 20 to 100 SB in the body of mammals.
An increase in the incidence of cancer and cardiovascular diseases with selenium deficiency, infertility in men and an increase in the risk of death from AIDS may be associated with a decrease in the biosynthesis of SB and disruption of the corresponding biochemical processes.
According to modern concepts, the general regulated form of selenium in the body is selenide, which is formed from selenocysteine ​​under the action of Sec-β-lyase. The precursor of selenocysteine ​​can be selenomethionine. Inorganic selenium (selenite) reacts with the reduced form of glutathione (GSH) also to form selenide. The latter is partially included in the biosynthesis of SB and tRNA as a result of a reaction with selenium phosphate synthetase (SPS), and is partially excreted from the body mainly in the form of methylated forms in urine and respiration. Phosphorylation of selenide is carried out with the participation of ATP. Regulation of the phosphorylation reaction of selenide determines the ability to deposit selenium - a phenomenon observed during microelement deficiency. Inhibition of the reaction leads to an increase in selenide concentration and, as a consequence, to an increase in selenium excretion. This situation occurs when selenium is available in quantities greater than those required for the synthesis of selenoproteins.
The absorption of selenium by the body occurs in the small intestine, among the segments of which the duodenum provides a slightly higher transport speed, from where low-molecular forms of selenium can pass into the blood within 1 minute after entering the intestine. Absorption of sodium selenite occurs differently from organic compounds. Experimental evidence indicates that selenium reacts nonenzymatically with GSH to form selenide diglutathione, which can serve as a substrate for γ-glutamyltransferase and is thus transported across cell membranes. Since the selenium status of experimental animals has almost no effect on the amount of absorption of administered selenite, it should be assumed that there is no regulatory absorption mechanism for this compound. The amount and distribution of SB in the organs and tissues of mammals depends on the specificity of their expression, the selenium status of the organism, the duration of selenium intake and the chemical form of selenium in the diet.
With selenium deficiency, the level of SB is reduced, but the inclusion of the microelement is carried out primarily in the most important proteins and tissues - reproductive and endocrine organs, the brain. Skeletal muscles and heart are supplied with selenium more slowly
M. Wenzel et al. (1971) determined the biological half-life of selenium in tissues. In particular, for muscles this period was 100 days, for liver - 50 days, kidneys - 32 days and for blood serum - 28 days.
Under conditions of recovery from the selenium deficiency state, GPX-GI activity reaches a maximum within 10 hours after the start of selenium administration, while cGPX activity begins to increase only after 24 hours and does not reach a maximum even after 3 days.
Homeostatic regulation of selenium levels in various organs and tissues leads to the fact that when high doses of selenium are administered, the level of SB exceeds that achieved with adequate consumption. In humans, pGPX activity reaches a maximum with consumption of only 50 μg of selenium per day.
When sodium selenite was administered to animals in high doses, no increase in enzyme activity was observed, despite a significant increase in the concentration of the microelement in plasma and erythrocytes, but even a slight decrease was noted.
With a decrease in the total selenium content in plasma and erythrocytes, the proportion of PHGPX increases, and the level of cGPX and hemoglobin in erythrocytes increases.
After administration of radioactive selenium, a significant part of it is bound by blood plasma proteins. It turned out that erythrocytes play a leading role in this process, since 75Se in the form of selenite penetrates extremely quickly through their membranes within a few seconds. Within 1-2 minutes, 50-70% of the total blood selenium is concentrated in red blood cells. The in vitro model shows the time dependence of selenium redistribution between blood elements. There is reason to believe that by 4 minutes the concentration of the microelement reaches its maximum. Then, within 15-20 minutes, almost all selenium leaves the erythrocytes, binding first to albumin and then to globulins in the blood plasma.
A selenium “pump” is present in red blood cells in humans and a number of animals. Under the influence of the glutathione-glutathione peroxidase system, selenite undergoes transformation with the formation of a selenium complex with glutathione. Upon subsequent reduction, selenium catalyzes the transport of electrons to oxygen. Having left the erythrocyte, possibly as part of the selenoglutathione complex, this microelement is fixed in plasma proteins. In addition, reduced glutathione peroxidase activity in erythrocytes appears to promote the formation of oxidative forms of proteins such as hemoglobin (HbSSG). Selenium deficiency can lead to hemolysis of red blood cells.
Selenium compounds have shown varying bioavailability. It was found that selenium contained in most of the studied compounds has lower bioavailability compared to sodium selenite.
Selenium is excreted from the body mainly through urine, feces and exhaled air (garlic odor). Among the routes of elimination, the first is dominant, and the last is characteristic of acute and chronic poisoning. In case of toxicosis, an alternative way of removing selenium can be considered its accumulation in hair and nails.
The concentration of selenium in urine changes significantly during the day, but most of the administered selenium is excreted within 24 hours, which makes it possible to use this indicator as a criterion for selenium supply, because it correlates well with the level of consumption of this microelement. Typically, about 40-50% of consumed selenium is excreted this way, but in some cases this value can reach 60%. Depending on the dose consumed, the concentration of selenium in urine can vary from 0.9 µg/l (endemic areas of China) to 3900 µg/kg (Venezuela).
A factor influencing the level of excretion is the chemical form of selenium. Inorganic salts are generally excreted more easily from the body, making them safer to consume than organic compounds. There is evidence indicating a low level of excretion of organic forms of selenium and, therefore, the greatest danger of poisoning when consuming abnormally high doses.
In a stress test, healthy volunteers with a daily twofold increase in the level of microelement intake took sodium selenite in doses of 100 - 800 mcg/day. leads to active excretion of excess selenium in the urine, reaching 80-90% of the intake.
When taking drugs of organic origin, the limit of selenium excretion in urine is reached at a dose of 400 mcg/kg.
Selenium deficiency causes a number of endemic diseases in humans and animals. “White muscle” disease (alimentary muscular dystrophy) is characterized by focal degeneration of varying severity and necrosis of skeletal and cardiac muscles of a non-inflammatory nature; it is prevented by the inclusion of selenium in the diet. Pathomorphological changes in this disease are characterized by profound disorders of the skeletal muscles and myocardium. In particular, a motley pathohistological picture is observed due to uneven plethora, dystrophic and necrobiotic changes in cardiomyocytes, often with phenomena of dystrophic calcification. According to A.P. Avtsyn (1972), the white color of the muscles is due to the disappearance of myoglobin and secondary coagulative necrosis of myocytes. Changes in the myocardium and skeletal muscles are of a degenerative-necrobiotic nature. Keshan disease is an endemic fatal cardiomyopathy characterized by arrhythmias, enlarged heart, focal myocardial necrosis, followed by heart failure. In patients suffering from this disease, abnormalities of erythrocyte membranes are detected. In the erythrocytes of sick children, the level of selenium, the activity of Na+, K+-ATPase, the fluidity of lipids and their membranes differ from the indicators of children in the control group living in the same region.
When conducted in Finland for 5 years, epidemiological studies on 11,000 men and women aged 35-59 years old found that during this period, 252 suffered myocardial infarction and 131 died from cardiovascular diseases. In all cases, the selenium level was 52 µg/l, in the control it was 55 µg/l. A number of studies carried out back in the 80s demonstrated that when the selenium concentration in the serum is below 0.4 µmol/l, the likelihood of myocardial infarction increases by 7 times, and at a content of 0.4-0.6 µmol/l - by 3 times.
In another study conducted under the same conditions, selenium levels were 62 μg/L for a group of deceased individuals. In the control 68 µg/l. The relative risk of death with plasma selenium concentrations less than 45 μg/L was 3.2.
In areas of Central Africa that are both deficient in selenium and iodine, endemic myxedematoid cretinism has been reported.
Experimental and clinical studies have shown that the etiology of cystic fibrosis of the pancreas (cystic fibrosis) is due to a deficiency of a number of elements, especially selenium, in the perinatal period. This disease is common among young children. In addition, with selenium deficiency, alimentary hepatosis is observed - necrotic changes in the liver, extensive edema and deposition of ceroid pigment in adipose tissue, and focal and diffuse infiltration in the intestines, stomach, mesentery and regional lymph nodes - idiopathic eosinophilic infiltration.
The first information about selenium is associated with manifestations of its toxicity caused by abnormally high consumption. There are several degrees of toxicity.
Acute toxicity occurs with short-term consumption of high doses of selenium and quickly leads to death. Signs: garlic breath, lethargy, excessive salivation, muscle tremors, myocarditis, etc.
Subacute toxicity is associated with the consumption of high doses of selenium over a significant period of time. Signs: blindness, ataxia, disorientation, difficulty breathing.
Chronic selenosis develops when moderately high amounts of selenium are consumed over several weeks or months.
Assessing the degree of toxicity of selenium compounds to humans is hampered by the lack of a selective and sensitive indicator of excess selenium intake into the human body. One possible indicator is alopecia and nail changes, as well as preferential accumulation of selenium in red blood cells compared to plasma.
A safe and sufficient daily intake of selenium is 50 – 200 mcg/day. The minimum requirement for selenium was established based on data for endemic regions of China: the smallest consumption of the microelement, at which the development of Keshan disease was not observed, was 19 and 14 mcg/day for men and women, respectively.
The physiological requirement for selenium is established by the consumption rate that provides maximum plasma GPX activity. For residents of the biogeochemical provinces of China with a deep selenium deficiency, this value is 40 μg/day. For Europeans, this level is 70 mcg for men and 55 mcg for women.
In Finland, taking into account many years of experience in the use of selenium-enriched fertilizers, a significantly higher level of selenium consumption is assumed to meet physiological needs, namely 120 μg/day, this value corresponds to the maximum activity of platelet GPX.
When calculating the RD (dose reference), based on the data obtained from studying endemic selenosis in China, take 853 mcg/day for a body weight of 55 kg. The introduction of an additional coefficient (x3) to take into account individual sensitivity gives a value of 5 μg of selenium per 1 kg of body weight per day, which corresponds to 350 μg/day for a body weight of 70 kg.