Selenium antagonist

Schrauzer, G.N., Effects of selenium antagonists on cancer susceptibility New aspects of chronic heavy metal toxicity, J UOEH 9, 208, 1987. 

Schrauzer G, White D, Schneider C. 1976. Inhibition of the genesis of spontaneous mammary tumors in C3H mice Effects of selenium and of selenium-antagonistic elements and their possible role in human breast cancer. Bioinorg Chem 6 265-270. 

Swanson AB, Wagner PA, Ganther HE, et al. 1974. Antagonistic effects of silver and tri-o-cresyl phosphate on selenium and glutathione peroxidase in rat liver and erythrocytes [Abstract], Fed Proc... 

Hall and Wolf [217] have proposed a hypothesis, concerning the pathogenesis of post-traumatic central nervous system ischaemia, which integrates an injury-induced rise in intracellular Ca2+, the increased synthesis of vasoactive prostanoids and progressive microvascular lipid peroxidation. The model used anaesthetised cats with a contusion injury to the lumbar spinal cord. Antioxidants, vitamin E and selenium, were compared with various Ca2 + antagonists, cyclo-oxygenase inhibitors, a thromboxane synthetase inhibitor and the stable prostacyclin analogue. The most impressive preservation of post-traumatic spinal cord blood flow was provided by the antioxidants. 

Regarding this selenium I have heard different opinions. One is that it is acting as an antagonistic agent, immobilizing for instance mercury. It may immobilize also cadmium, because the selenites in question are quite insoluble. We know that in lakes where we have higher selenium content there is less mercury in the fish. This is of course not conclusive, but that may be an idea... 

Yes, it is right that selenium has some antagonistic effects on other poisoning elements, and also I can mention interference with vitamin E, so that a combination of selenium and vitamin E can give quite a good result. The fact is that we know too little about it, but in other ways this is a question for further research. 

The apparent affinity for zinc metallothionein may someday be found to be useful as an antidote for cadmium toxicity. Antagonists to cadmium toxicity include a pretreatment with selenium and zinc. It is believed that this pretreatment allows cadmium to displace zinc in the zinc metallothionein. 

Potassium dichromate and atrazine may increase the toxicity of mercury, although these effects have been noted only with metallic and inorganic mercury. Ethanol increases the toxicity of methylmercury in experimental animals. Vitamins D and E, thiol compounds, selenium, copper, and possibly zinc are antagonistic to the toxic effects of mercury. 

Methionine and Vitamin E. Combinations of methionine and vitamin E have been found to be antagonistic to selenium toxicity. In one study, selenium concentrations in the liver and kidneys of rats fed selenium-containing diets with methionine and vitamin E were less than the concentrations found in the livers and kidneys of rats fed selenium with either methionine or vitamin E alone (Levander and Morris 1970). The results are compatible with the hypothesis that methionine detoxifies selenium by forming methylated derivatives of selenium that are eliminated in the urine and in expired air (see Section 3.4.4) or that methionine and selenomethionine are in the same pool of amino acids and that by increasing the amount of methionine relative to selenomethionine, the probability of selenomethionine being randomly inserted into proteins during synthesis decreases (Stadtman 1977,1980,1983,1987, 1990). As discussed in Section 3.11, methionine administered as an antidote for acute selenium toxicity in rats was ineffective (Lombeck et al. 1987). This result supports a mechanism of action involving protein synthesis rather than a methylation mechanism hypothesis. 

One report indicates a nontoxic dose of silver acetate in rats minimizes effects of acute selenium toxicity. However, the body burden of selenium in several organs increased with treatment with silver acetate. It is postulated that this antagonistic effect may be due to the formation and disposition of silver selenides which are relatively insoluble and nontoxic (Eybl et al. 1992). 

Zhang Y, Xiao H. 1998. Antagonistic effect of calcium, zinc and selenium against cadmium induced chromosomal aberrations and micronuclei in root cells of Hordeum vulgare. Mutat Res 420 1-6. 

Sulfur-containing compounds such as alpha-lipoic acid, methylsulfonylmethane, glutathione, N-acetylcysteine and cysteine are effective against oxidative stress and cell damage caused by free radicals (Bray and Taylor 1993, Pollack et al. 1996). Alpha-lipoic acid increases the antioxidant potency of further antioxidants such as vitamins E and C (Kagan et al. 1992). The course of acute pancreatitis is dramatically impaired in cases of very low antioxidant status. Whereas the sulfur antagonist selenium reduced remarkably the death rate (Kulinski et al. 1995), methionine was also used successfully in the treatment of this disease (Uden et al. 1990). 

Sulfur has an antagonistic effect on several essential trace elements. Excessive amounts of sulfur can induce a secondary deficiency of copper (mainly in animals), cobalt and selenium. Ho vever, not only the sulfur amino acid cysteine but also sulfate eliminates the adverse effects of copper-, cobalt-or selenium-based toxicities (Baker and Czarnecki-Maulden 1987). Sulfate increases the urinary loss of selenate, but not of selenite this explains the assumption that there is a direct antagonism between sulfate and selenate (Schrauzer 1998). 

Synergistic effects such as those of cadmium and cyanide or of lead and chromium are just beginning to be recognized. Antagonistic effects such as those between selenium and arsenic, fluoride, mercury, or lead cadmium and zinc or selenium copper and zinc or molybdenum and iron and manganese or zinc have only recently been observed. 

Selenium and arsenic are antagonists in several animal species. Dietary arsenic, as arsenate, alleviates the toxic effects of selenium, as seleno-DL-methionine, on mallard (Anas platyrhynchos) reproduction, duckling growth, and survival. Mallard ducklings fed arsenate in the diet at 200.0 mg As/kg ration were protected against the toxic effects... 

It is impossible to discuss the effects of vitamin E on the health and wellbeing of ruminant animals without taking into consideration many other nutritional and environmental factors. These include the effects of the amount and nature of the dietary supply of fat, the presence in food of specific antagonists to vitamin E, the incidence of stress in the animals concerned, and the dietary concentration of selenium. The veterinary and agricultural implications of the discovery that selenium is an essential element (Schwarz and Foltz, 1957 Patterson et al., 1957), and that it is effective in the prevention of some of those syndromes in laboratory animals which can be prevented by giving vitamin E, were soon realized, and at the present time considerable work has been done and is in progress on these aspects. These are reviewed. 

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