Cobalamin neuropathy. Is S-adenosylhomocysteine toxicity a factor?
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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.
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2019 ◽
1970 ◽
Vol 28
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pp. 26-27
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1983 ◽
Vol 41
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pp. 788-789
1982 ◽
Vol 40
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pp. 44-45
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1995 ◽
Vol 53
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pp. 958-959
1996 ◽
Vol 26
(9)
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pp. 1092-1097
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