Abstract
Animals are known to convert inorganic selenium to less toxic methylated compounds such as dimethylselenide (DMSe) and trimethylselenonium (TMSe). This study investigated the role of vitamin B 12, a cofactor of methionine synthetase, in selenium methylation in the rat. Vitamin B 12-depleted rats expired 16% of dosed 75Se-selenite as DMSe compared to 45% for control rats and excreted less TMSe in the urine (6.1% of dose) than control (9% of dose) rats. At the same time, higher ( p < 0.05) tissue (liver, kidney, muscle) selenium levels and lower ( p <0.05) blood selenium levels were found in vitamin B 12-deficient rats. Primary hepatocytes from vitamin B 12-deficient rats volatilized 15% of selenite in incubation medium in 5 hr as compared to 49% in hepatocytes from control rats. Hepatocytes from vitamin B 12-deficient rats were less resistant to selenite toxicity. In vitro methylation of selenium with liver extract from vitamin B 12-deficient rats showed one-third to one-half the rate of volatilization of selenium as compared to control rats. Sadenosylmethionine was required for this reaction. These results show that vitamin B 12 deficiency significantly decreases the ability of rats to methylate selenium.
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