Nitrous oxide induced vitamin B12 deficiency: measurement of methylation reactions in the fruit bat (Rousettus aegyptiacus)

Int J Biochem. 1986;18(2):199-202. doi: 10.1016/0020-711x(86)90158-8.


Nitrous oxide induced inhibition of methionine synthetase activity has been proposed as a suitable model for the myelopathy associated with vitamin B12 deficiency. This suggests a defect in methyl group metabolism. The fruit bat has been used previously as a model for dietary induced vitamin B12 deficiency. However in the nitrous oxide treated fruit bat with neurological symptoms: No changes in [14C]ethanolamine incorporation into liver and brain phospholipids could be detected. No changes in synaptosomal and myelin lipid methylation could be shown. No differences in the rate of synaptosomal and myelin protein methylation could be measured. Therefore the fruit bat myelopathy is not related to a methyl group transfer deficiency.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain / metabolism*
  • Carbon Radioisotopes
  • Chiroptera / metabolism*
  • Ethanolamine
  • Ethanolamines / metabolism
  • In Vitro Techniques
  • Liver / metabolism*
  • Methylation
  • Nitrous Oxide
  • Vitamin B 12 Deficiency / chemically induced
  • Vitamin B 12 Deficiency / metabolism*


  • Carbon Radioisotopes
  • Ethanolamines
  • Ethanolamine
  • Nitrous Oxide