| pubmed-article:10327178 | pubmed:abstractText | Homocyteine (HC) induces neurotoxicity through overstimulation of N-methyl-D-aspartate (NMDA) receptors in cortical neurons. Due to its high reactivity, the sulfhydryl group of HC may react with nitric oxide (NO). In the present study S-nitrosation decreased the homocysteine-evoked LDH releases from rat cortical neuronal cultures. Like HC, S-nitrosohomocysteine increased the intracellular calcium concentration ([Ca2+]i) via NMDA receptor. However, S-nitrosohomocysteine was much less efficacious than HC for the increase of [Ca2+]i. Elevation of the glycine concentration to 50 microM significantly increased the maximal calcium response of S-nitrosohomocyteine, but not high enough to match that of HC in the presence of the same concentration of glycine. S-nitrosohomocysteine partially decreased the NMDA calcium responses in the presence of 1 and 50 microM glycine, at least in part via the redox-modulatory site(s) of the NMDA receptor. These data indicate that NO ameliorates the potential, adverse properties of HC via S-nitrosylation in the pathogenesis of hyperhomocysteinemia. | lld:pubmed |
