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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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