Tissue folates in fruit bats (Rousettus aegyptiacus) with nitrous oxide-induced vitamin B12 deficiency and neurological impairment.

1. Long-term exposure of the fruit bat Rousettus aegyptiacus to nitrous oxide, which inactivates methylcobalamin, leads to neurological impairment and ataxia. 2. In N2O-exposed animals, liver concentrations of total folates and methyl folates decreased to less than one-fifth that of control animals. Pediococcus cerevisiae-active folates were also reduced. 3. In brain, there were no changes in total or methyl folates, but P. cerevisiae-active folates were lower in N2O-exposed animals. 4. Supplementation with methionine retarded the development of neurological impairment and the fall in liver total and methyl folates, but not that in P. cerevisiae-active folates. 5. Supplementation with serine failed to retard the development of neurological impairment or fall in hepatic folates. 6. The present results suggest that the N2O-induced neurological impairment in the bat is not related to depletion of cerebral folates, but do not exclude changes in the subcellular distribution of folates.