Protective Effects of Methyl B12 In Retinal Cells
Protective
Effects of Methylcobalamine, A Vitamin B12 Analogue,
Against Glutamate-induced Neurotoxicity in Retinal
Cell Culture
Kikuchi
M Kashii S Honda Y Tamura Y Kaneda K Akaike,
Invest Ophthalmol Vis Sci (1997 Apr) 38(5):848-54
Purpose:
To examine the effects of methylcobalamine on
glutamate- induced neurotoxicity in the cultured
retinal neurons. Methods: Primary cultures obtained
from the fetal rat retina (gestation days 16 to 19)
were used for the experiment. The neurotoxicity was
assessed quantitatively using the trypan blue
exclusion method. Results: Glutamate neurotoxicity was
prevented by chronic exposure to methylcobalamine and
S-adenosylmethionine (SAMe), which is formed in the
metabolic pathway of methylcobalamin. Chronic exposure
to methylcobalamine and SAMe also inhibited the
neurotoxicity induced by sodium nitroprusside that
release nitric oxide. By contrast, acute exposure to
methylcobalamine did not protect retinal neurons
against glutamate neurotoxicity. Conclusions: Chronic
administration of methylcobalamine protects cultured
retinal neurons against N-methyl-D- aspartate-receptor-mediated
glutamate neurotoxicity, probably by altering the
membrane properties through SAMe-mediated methylation.
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