Selenium toxic effects

Hadjimarkos DM. 1969a. Selenium toxicity Effect of fluoride. Experientia 25 485-486. 

Control of metalloid content in natural objects, foodstuff and pharmaceuticals is an important task for modern analytical chemistry. Determination of elements such as Arsenic is necessary for evaluation of object toxicity, since their content in environment may exceed MCL (maximum contaminant level), posing hazard to human health. Elements such as Selenium in definite doses are healthy, but in greater quantities they produce toxic effect. 

Additional fundamental and basic research is required on selenium metabolism, physiology, recycling, interactions with other compounds or formulations, and chemical speciation in order to elucidate its nutritive role as well as its toxic effects. 

Chapman, D.C. 1992. Failure of gas bladder inflation in striped bass effect on selenium toxicity. Arch. Environ. Contamin. Toxicol. 22 296-299. 

Ostadalova, I. and A. Babicky. 1980. Toxic effect of various selenium compounds on the rat in the early postnatal period. Arch. Toxicol. 45 207-211. 

Stable, e.g. selenium compounds.6 The selenate ion exerts a toxic effect, but does not undergo any further chemical change in the plant. 

Selenium is readily available in a variety of foods including shrimp, meat, dairy products, and grains, with a recommended daily intake of 55 to 70 jug. It occurs in several forms with Se+6 being biologically most important. Selenium is readily absorbed by the intestine and is widely distributed throughout the tissues of the body, with the highest levels in the liver and kidney. It is active in a variety of cellular functions and interacts with vitamin E. Selenium appears to reduce the toxic effects of metals such as cadmium and mercury and to have anticarcinogenic activity. Selenium produces notable adverse effects both in deficiency and excess thus recommended daily intake for adults is approximately 70 Jg/day but should not exceed 200 pg/day. 

Larger particles (several micrometers in size) are deposited in the ciliated portion and are cleared from the respiratory system by muco-ciliary action into the gastronomical tract, but may produce systemic toxic effects by absorption in body fluids. Finer particles reach the lower non-ciliated portion of the lungs, are cleared very slowly, and are responsible for diseases such as pneumoconiosis and lung cancer. Metallic lead (Pb), tellurium ( ), selenium (Se), and platinum (Pt) are known to cause both systemic and respiratory toxicity in laboratory animals and several cases of acute and chronic poisoning among metal workers have also been documented. 

Populations that are unusually susceptible to toxic effects of silver exposure are those that have a dietary deficiency of vitamin E or selenium, or that may have a genetically based deficiency in the metabolism of these essential nutrients. Individuals with damaged livers may also be more susceptible to the effects of silver exposure. In addition, populations with high exposures to selenium may be more likely to develop argyria. Furthermore, some individuals may exhibit an allergic response to silver. 

Kim, Y.Y. and Mahan, D.C. 2001. Comparative effects of high dietary levels of organic and inorganic selenium on selenium toxicity of growing-finishing pigs. J. Anim. Sci. 79, 942-948. 

Selenium is mostly found in arid environments under irrigated agriculture. Selenium has toxic effects at high dose levels, but at low dose levels is an essential nutrient. It is classified in the EPA s Group D (not classifiable), and because of its potential chronic health effects, it is regulated by the U.S. government. 

Imura N, Naganuma A, Satoh M, Koyama Y. Depression of toxic effects of anticancer agents by selenium or pretreatment with metallothionein inducers. J UOEH 1987 9(Suppl) 223-9. 

It should be noted that in the majority of the above mentioned studies, metal-induced renal injury was considered as if exposure occurred to only one metal at a time. In reality it is clear that environmental and occupational exposure may involve several metals at the same time and in varying concentrations [34]. It has been shown that with combined exposure various metals may interact with each other and that one metal may alter the potential toxicity of another in either a beneficial or deleterious way. As an example, whilst arsenic has been shown to worsen cadmium-induced nephrotoxicity, data from experimental studies have shown that selenium may protect against the renal effects induced by cadmium [52]. Other studies have shown that the iron status may alter the toxic effects of aluminium at the level of the bone and the parathyroid gland [53,54], whilst in a recent increased lead accumulation was associated with disturbances in the concentration of a number of essential trace elements [55]. 

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. 

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