S-nitrosation ameliorates homocysteine-mediated neurotoxicity in primary culture of rat cortical neurons

Research output: Contribution to journalArticle

Abstract

The reactivity of the sulfhydryl (thiol) group of homocysteine has been associated with an increased risk of atherosclerosis, thrombosis and stroke. Thiols also react with nitric oxide (NO, an endothelium-derived relaxing factor (EDRF)), forming S-nitrosothiols that have been reported to have potent vasodilatory and antiplatelet effects and been expected to decrease adverse vascular effects of homocysteine. The present study was aimed to investigate whether the S-nitrosation of homocysteine modulates the neurotoxic effects of homocysteine. An 18 hour-exposure of cultured rat cortical neurons to homocysteine (>1 mM) resulted in a significant neuronal cell death. At comparable concentrations (<10 mM), however, S-nitrosohomocysteine did not induce neuronal cell death. Furthermore, S-nitrosohomocysteine partially blocked NMDA-mediated neurotoxicity. S-nitrosohomocysteine also decreased NMDA-mediated increases in intracellular calcium concentration. The present data indicate that in brain nitric oxide produced from neuronal and nonneuronal cells can modulate the potential, adverse properties of homocysteine.

Original languageEnglish
Pages (from-to)169-175
Number of pages7
JournalKorean Journal of Pharmacology
Volume32
Issue number2
Publication statusPublished - 1996

Keywords

  • S-nitrosohomocysteine
  • calcium
  • cortical neuron
  • homocysteine
  • neurotoxicity
  • primary culture

ASJC Scopus subject areas

  • Pharmacology

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