Published online by Cambridge University Press: 09 March 2007
1. Long-term exposure of the fruit bat Rousettus aegyptiacus to nitrous oxide, which inactivates methylco balamin, leads to neurological impairment and ataxia.
2. In N2, O-exposed animals, liver concentrations of total folates and methyl folates decreased to less than one fifth that of control animals. Pediococcus cerevisiue-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 N2, O-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.