Cytotoxicity induced by grape seed proanthocyanidins: Role of nitric oxide

Z. H. Shao, C. W. Hsu, W. T. Chang, G. B. Waypa, J. Li, D. Li, C. Q. Li, T. Anderson, Y. Qin, P. T. Schumacker, L. B. Backer, T. L. Vanden Hoek

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37 引文 斯高帕斯(Scopus)


Grape seed proanthocyanidin extract (GPSE) at high doses has been shown to exhibit cytotoxicity that is associated with increased apoptotic cell death. Nitric oxide (NO), being a regulator of apoptosis, can be increased in production by the administration of GSPE. In a chick cardiomyocyte study, we demonstrated that high-dose (500 μg/ml) GSPE produces a significantly high level of NO that contributes to increased apoptotic cell death detected by propidium iodide and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining. It is also associated with the depletion of intracellular glutathione (GSH), probably due to increased consumption by NO with the formation of S-nitrosoglutathione. Co-treatment with L-NAME, a NO synthase inhibitor, results in reduction of NO and apoptotic cell death. The decline in reduced GSH/oxidized GSH (GSSG) ratio is also reversed. N-Acetylcysteine, a thiol compound that reacts directly with NO, can reduce the increased NO generation and reverse the decreased GSH/GSSG ratio, thereby attenuating the cytotoxicity induced by high-dose GSPE. Taken together, these results suggest that endogenous NO synthase (NOS) activation and excessive NO production play a key role in the pathogenesis of high-dose GSPE-induced cytotoxicity.

頁(從 - 到)149-158
期刊Cell Biology and Toxicology
出版狀態已發佈 - 5月 2006

ASJC Scopus subject areas

  • 毒理學
  • 細胞生物學
  • 健康、毒理學和誘變


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