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Methylation Deficiency Causes Vitamin B 12 ‐Associated Neuropathy in the Pig
Author(s) -
Weir D. G.,
Keating S.,
Molloy A.,
McPartlin J.,
Kennedy S.,
Blanchflower J.,
Kennedy D. G.,
Rice D.,
Scott J. M.
Publication year - 1988
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1988.tb01184.x
Subject(s) - ataxia , methionine , methylation , endocrinology , medicine , concomitant , vitamin , vitamin b , vitamin b12 , biology , chemistry , biochemistry , amino acid , neuroscience , gene
Pigs were treated with N 2 O which is known to impair vitamin B 12 function in vivo. Such pigs demonstrated an inability to gain weight, progressive ataxia, and spinal neuropathy. The ataxia was totally and the neuropathy partially preventable by dietary methionine supplementation. Methionine synthase activity was inhibited in both the liver and brain. There was a marked elevation of S ‐adenosylhomocysteine in the neural tissues and a concomitant failure of S ‐adenosylmethionine to rise and thus maintain the methylation ratio, except when supplementary dietary methionine was added. In contrast, the methylation ratio in the rat was affected to a lesser extent. The neuropathy, it is suggested, is caused by raised S ‐adenosylhomocysteine levels in neural tissue; as a result, the methylation ratio is inverted and S ‐adenosylmethionine‐dependent methylation reactions are inhibited.