The interactions of selenium with cadmium and mercury.
摘要:
The interactions occurring between selenium (7782492), cadmium (7440439), and mercury (7439976) compounds in the human and animal organisms are reviewed. The toxicity of selenium is influenced by factors such as species, sex, age, and diet. A methionine deficiency enhances the toxic influence exerted by selenium. The addition of arsenite to rat diets counteracts the toxicity of seleniferous grain. Tungsten, germanium, and antimony are also effective antagonists of the toxicity of dietary selenium. Mercury cation administration a few hours after the intake of anionic selenite (14124675) increases selenium compound toxicity. In experimental animals, simultaneous or prior injection with selenium, usually in the form of anionic selenite, protects against many of the acute effects of cationic cadmium. The teratogenic and fetotoxic effects of cationic cadmium observed in pregnant animals appear to be the result of transport process inhibition due to cadmium uptake into the placenta. Cationic cadmium is associated with extensive testicular damage in mice. Selenite (most probably, in the form of its metabolites) protects against testicular necrosis induced by cationic cadmium. The toxicity of methylmercury (22967926), which is the only mercurial that selectively damages the human nervous system, exhibits significant species related differences, with the nervous system being the site of major injury. Selenite inhibits the neurotoxic effects of methylmercury in Japanese-quail, delaying the development of coordination disorders, and also exerts a protective influence against methylmercury intoxication in rats. Both truncal ataxia and death due to mercury poisoning are delayed in cats when selenium is introduced. The authors conclude that the lack of appropriate kinetic data does not permit the definition of the changes occurring in methylmercury kinetics as a result of selenite introduction, although it is certain that the protective effect of the latter against the former is not the result of a decrease in the methylmercury concentration in place in the nervous system.
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关键词:
Saccharomyces cerevisiae DNA Damage Chromosome Deletion DNA DNA, Fungal Blotting, Southern Densitometry G1 Phase DNA Repair Recombination, Genetic
DOI:
10.3109/10408448009037490
被引量:
年份:
1980
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