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.
D000818:Animals; D001921:Brain / Q000378:metabolism; D002685:Chiroptera; D005492:Folic Acid / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D008715:Methionine / Q000008:administration & dosage; D009422:Nervous System Diseases / Q000139:chemically induced / Q000178:diet therapy / Q000378:metabolism*; D009609:Nitrous Oxide; D012694:Serine / Q000008:administration & dosage; D014806:Vitamin B 12 Deficiency / Q000139:chemically induced / Q000378:metabolism*
D012694:Serine; D005492:Folic Acid; D008715:Methionine; D009609:Nitrous Oxide