COBALAMIN NEUROPATHY - IS S-ADENOSYLHOMOCYSTEINE TOXICITY A FACTOR

被引:23
|
作者
VIEIRAMAKINGS, E
METZ, J
VANDERWESTHUYZEN, J
BOTTIGLIERI, T
CHANARIN, I
机构
[1] NORTHWICK PK HOSP & CLIN RES CTR,MRC,CLIN RES CTR,HAEMATOL SECT,HARROW HA1 3UJ,MIDDX,ENGLAND
[2] S AFRICAN INST MED RES,SCH PATHOL,DEPT HAEMATOL,JOHANNESBURG 2000,SOUTH AFRICA
[3] UNIV WITWATERSRAND,JOHANNESBURG 2001,SOUTH AFRICA
关键词
D O I
10.1042/bj2660707
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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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收藏
页码:707 / 711
页数:5
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