Effect of N2O treatment/vitamin B12 deficiency in pigs on tissue concentrations of odd-numbered, branched-chain fatty acids.

Activity of the vitamin B12-dependent enzyme, methylmalonyl CoA mutase, was measured in the tissues of pigs, fed a diet which was low in cobalt and vitamin B12, and which were intermittently exposed to nitrous oxide until they displayed marked ataxia. Methylmalonyl CoA mutase activity was reduced in liver, kidney and brain. However, the methylmalonic acid concentration was reduced in liver and heart, in marked contrast to the expected increase which was only observed in brain. Liver and kidney also showed an unexpected reduction in the concentration of C17 odd-numbered fatty acids, possibly as a consequence of reduced propionate availability. Brain however, which had elevated methylmalonic acid concentrations showed no change in either odd-numbered or branched-chain fatty acids. These results suggest that nitrous oxide-induced neuropathy does not occur as a result of misincorporation of odd-numbered/branched-chain fatty acids in brain.