Metals on Selenium Metabolism

Silver and mercury were shown to markedly reduce the absorption of selenium in rats when the inorganic salts of these elements were given orally (Whanger, 1976). Cadmium had a lesser effect on selenium absorption, and lead had no effect. Using lettuce leaves labeled either intrinsically or extrinsically with and Se, the absorption of Se 

The influence of selected heavy metals on the toxicity of some metabolites of selenite has been studied by Parizek et al, (1971). Cadmium had no effect on the toxicity of dimethylselenide, but a strong sex-linked interaction between mercury and this compound was found. The toxicity of both dimethylselenide and the trimethylselenium ion was greatly enhanced by the administration of mercuric compounds to male rats but was unaffected in females. Part of the reason for these sex-linked differences may be that the urinary excretion of trimethylselenium ions is under the control of anabolic steriods (Parizek et al., 1974). However, this does not fully explain all of these sex-linked effects. 

The lack of influence of cadmium on GSH-Px activity in our studies is consistent with the results of Prohaska et al. (1977) but is at variance with those of Omaye and Tappel (1975). The reasons for this disagreement are not readily apparent. In work with rat testis cytosol, two different GSH-Px activities were found when assayed with cumene hydroperoxide (Prohaska et al, 1977). The larger MW species eluted with the void volume on Sephadex G-150 columns and incorporated Se from selenite, but the smaller one (42,000 MW) did not incorporate Se from radioactive selenite. When CdCl2 was given to rats injected 4 wk previously with a tracer dose of Se-selenite, Sephadex G-150 chromatography of testis cytosol showed that most of the ° Cd was eluted in a major peak of 34,000 MW, but very little Cd was found in association with a major Se peak (140,000 MW) or with GSH-Px activity. Thus, under homeostatic conditions, cadmium does not appear to bind to the major selenium-containing protein or to GSH-Px in the testes. 

In contrast to the infiuence of inorganic mercury, methylmercury has only minor effects upon GSH-Px activity (Whanger, 1981). Methylmercury had no significant effect upon GSH-Px in the testes, and only those rats fed 25 ppm methylmercury had significantly lower GSH-Px activity in erythrocytes, kidneys, brain, and livers. Additions of 7.5 or 15 ppm methylmercury to the diet had no significant effect on the activity of this enzyme in any of these tissues. The slight reduction in GSH-Px activity 

The interaction of selenium and methylmercury in the brain appears to be very complex. Despite the clear protective effect of selenite on methylmercury toxicity, selenium increases the mercury content of brain (Prohaska and Ganther, 1977 Chen et al, 1975a). Methylmercury tends to cause a shift in the concentration of selenium from the cytosol to the mitochondrial fraction in the brain. Gel filtration of the brain cytosol, however, revealed that mercury followed a pattern more closely related to protein than to selenium (Prohaska and Ganther, 1977). Therefore, the mechanism of the protective effect of selenium against methylmercury toxicity is still a subject for speculation. 

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