title: Effect of vitamin B12 status on selenium methylation and toxicity in rats: in vivo and in vitro studies.
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 B12, a cofactor of methionine synthetase, in selenium methylation in the rat. Vitamin B12-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 B12-deficient rats. Primary hepatocytes from vitamin B12-deficient rats volatilized 15% of selenite in incubation medium in 5 hr as compared to 49% in hepatocytes from control rats. Hepatocytes from vitamin B12-deficient rats were less resistant to selenite toxicity. In vitro methylation of selenium with liver extract from vitamin B12-deficient rats showed one-third to one-half the rate of volatilization of selenium as compared to control rats. S-adenosylmethionine was required for this reaction. These results show that vitamin B12 deficiency significantly decreases the ability of rats to methylate selenium.
authors.affiliation: Department of Agricultural Chemistry, Oregon State University, Corvallis 97331.
authors.forename: C L
authors.initials: CL
authors.lastname: Chen
authors.forename: P D
authors.initials: PD
authors.lastname: Whanger
mesh_terms: D000818:Animals; D066298:In Vitro Techniques; D008099:Liver / Q000378:metabolism; D008297:Male; D008745:Methylation; D008764:Methylmalonic Acid / Q000652:urine; D051381:Rats; D017207:Rats, Sprague-Dawley; D012643:Selenium / Q000378:metabolism* / Q000633:toxicity*; D014806:Vitamin B 12 Deficiency / Q000378:metabolism*; D014835:Volatilization
chemical_list: D008764:Methylmalonic Acid; D012643:Selenium