Vitamin B12 neuropathy is not due to failure to methylate myelin basic protein

• Published in: Journal of the neurological sciences Vol. 72; no. 1; pp. 113 - 117
• Main Authors: DEACON, R, PURKISS, P, GREEN, R, LUMB, M, PERRY, J, CHANARIN, I
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Science 1986
• Subjects: Animals; Arginine - metabolism; Biological and medical sciences; Brain Diseases - metabolism; Chiroptera; Cycloleucine - pharmacology; Disease Models, Animal; Liver - metabolism; Medical sciences; Metabolic diseases; Methylation; Myelin Basic Protein - metabolism; Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...); Rats; Rats, Inbred Strains; Vitamin B 12 - blood; Vitamin B 12 Deficiency - metabolism; Animal model; Vertebrata; Nervous system diseases; Mammalia; Rat; Pathogenesis; Rodentia; Vitamin deficiency; Metabolic diseases; Neuropathy; Cyanocobalamin
• ISSN: 0022-510X; 1878-5883
• DOI: 10.1016/0022-510X(86)90040-7

It has been proposed that the biochemical lesion in subacute combined degeneration of the cord due to vitamin B12 deficiency, is impaired methylation of residue 107 (arginine) in myelin basic protein. We have examined myelin basic protein in brains of rats in which vitamin B12 was inactivated by exposure to nitrous oxide for up to 7 days. In addition brains of fruit bats in which vitamin B12 neuropathy had been produced by feeding washed, and hence vitamin B12-free fruit, were examined. There was no difference in the methylation of arginine 107 in myelin basic protein in these animals as compared to healthy control animals. Rats given an inhibitor of transmethylation reactions (cycloleucine) showed the expected fall in methylation of myelin basic protein.