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Cobalamin neuropathy. Is S-adenosylhomocysteine toxicity a factor?
E Vieira-Makings1, J Metz, J Van der Westhuyzen
1Department of Haematology, School of Pathology, South African Institute for Medical Research, Johannesburg.
The Biochemical Journal
|March 15, 1990
Abstract:
Cobalamin neuropathy was produced in cape fruit bats (Rousettus aegyptiacus) by a cobalamin-free diet combined with intermittent exposure to nitrous oxide, which inactivates cobalamin. There were no significant differences in S-adenosylmethionine/S-adenosylhomocysteine ratios in the central nervous system of cobalamin-deficient and cobalamin-replete bats. Taken with other data there are no grounds of support for a hypothesis that cobalamin neuropathy is the result of impaired methylation, however produced.