EFFECT OF NITROUS-OXIDE ON NICKEL DEPRIVATION IN RATS

Because nickel may have a biological function in a pathway in which vi tamin B12 is important, an experiment was performed to determine the e ffects of nitrous oxide exposure in rats deprived of nickel. Exposure to nitrous oxide (N2O) causes inactivation of cobalamin and a subseque nt decrease in the vitamin B12-dependent enzymes methionine synthase a nd methylmalonyl CoA mutase. Rats were assigned to dietary groups of 1 2 in a factorially arranged experiment with dietary variables of nicke l (0 or 1 mug/g) and vitamin B12 (0 or 50 ng/g). After 6 wk, one-half of the rats from each dietary group were exposed to 50% N2O/50% O2 for 90 min/d for the last 28 d of the experiment. Vitamin B12, N2O, or th eir interaction had numerous effects; classical findings included N2O- induced reduction in plasma vitamin B12 and decreases in the vitamin B 12-dependent enzymes. Inactivation of vitamin B12 by N2O, however, did not exacerbate signs of nickel deprivation, possibly because the rats were able to metabolically compensate to N2O exposure.