Cobalamin neuropathy. Is S-adenosylhomocysteine toxicity a factor?
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.
Vieira-Makings
E
E
Department of Haematology, School of Pathology, South African Institute for Medical Research, Johannesburg.
Metz
J
J
Van der Westhuyzen
J
J
Bottiglieri
T
T
Chanarin
I
I
D000818:Animals; D001923:Brain Chemistry; D002685:Chiroptera; D002851:Chromatography, High Pressure Liquid; D006710:Homocysteine / Q000031:analogs & derivatives*; D008099:Liver / Q000032:analysis; D008715:Methionine / Q000032:analysis; D009468:Neuromuscular Diseases / Q000150:complications / Q000378:metabolism*; D012435:S-Adenosylhomocysteine / Q000378:metabolism*; D012436:S-Adenosylmethionine / Q000032:analysis; D014633:Valine / Q000032:analysis; D014806:Vitamin B 12 Deficiency / Q000150:complications / Q000378:metabolism*
D006710:Homocysteine; D012436:S-Adenosylmethionine; D012435:S-Adenosylhomocysteine; D008715:Methionine; D014633:Valine