Inhibition of vitamin B12 metabolism by OH-cobalamin c-lactam in rat oligodendrocytes in culture: a model for studying neuropathy due to vitamin B12 deficiency.

Abstract:

:Vitamin B12 is implicated in methylation processes. Myelin basic protein is methylated on one arginine group. A defect in methylation could produce an unstable protein, leading to neurological disorders. In order to study myelin basic protein, we have developed the cultures of newborn rat oligodendrocytes in vitamin B12-depleted medium. As these cells do not grow without serum, vitamin B12 is always present. We overcame this problem by using OH-cobalamin c-lactam, an antagonist of B12. To ensure that the system was vitamin B12 deficient, we measured the concentrations of homocysteine and methylmalonic acid whose accumulations reflect a vitamin B12 deficiency. Methylmalonic acid was measured by mass spectrometry and homocysteine by HPLC. We obtained a powerful model for studying the influence of B12 deficiency on the synthesis of myelin compounds.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Sponne IE,Gaire D,Stabler SP,Droesch S,Barbé FM,Allen RH,Lambert DA,Nicolas JP

doi

10.1016/s0304-3940(00)01243-x

keywords:

subject

Has Abstract

pub_date

2000-07-21 00:00:00

pages

191-4

issue

3

eissn

0304-3940

issn

1872-7972

pii

S030439400001243X

journal_volume

288

pub_type

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