Cytoprotective effect of reduced glutathione in hydrogen peroxide-induced endothelial cell injury

S. H. Chen; H. L. Wu; M. T. Lin; C. J. Jen; L. Y C Wing; H. Y. Lei; C. J. Tsao; W. C. Chang

doi:10.1016/0952-3278(92)90087-Y

Cytoprotective effect of reduced glutathione in hydrogen peroxide-induced endothelial cell injury

S. H. Chen, H. L. Wu, M. T. Lin, C. J. Jen, L. Y C Wing, H. Y. Lei, C. J. Tsao, W. C. Chang

Research output: Contribution to journal › Article › peer-review

11 Citations (Scopus)

Abstract

The kinetic effects of hydrogen peroxide (H₂O₂) on cultured endothelial cells isolated from bovine carotid artery were studied. The cytoprotective effects of glutathione (GSH) on H₂O₂-induced cell injury were also investigated. H₂O₂-induced a dose- and time-dependent cell injury in cultured endothelial cells. H₂O₂-induced cell injury was blocked by simultaneous treatment by catalase, but not by superoxide dismutase. H₂O₂ also induced endogenous PGI₂ biosynthesis, and the maximum PGI₂ production was reached after 1 h treatment. Stimulation of PGI₂ production was parallel with arachidonate release from H₂O₂-treated cells. However the prostaglandin biosynthesis enzyme activity in cells was inhibited by H₂O₂ treatment. When the cells were treated with GSH, the intracellular GSH reached a plateau after 3 h treatment. Both H₂O₂-induced cell injury and PGI₂ production were significantly inhibited by the 3 h pretreatment with GSH. The cytoprotective effect of GSH was completely inhibited by buthionine sulfoximine which is a specific inhibitor of γ-glutamylcysteine synthetase. The results indicate that the cytoprotective effect of GSH on H₂O₂-induced cell injury in cultured bovine carotid artery endothelial cells depends on the increase in intracellular GSH content.

Original language	English
Pages (from-to)	299-305
Number of pages	7
Journal	Prostaglandins Leukotrienes and Essential Fatty Acids
Volume	45
Issue number	4
DOIs	https://doi.org/10.1016/0952-3278(92)90087-Y
Publication status	Published - 1992
Externally published	Yes

ASJC Scopus subject areas

Clinical Biochemistry
Endocrinology, Diabetes and Metabolism

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/0952-3278(92)90087-Y

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title = "Cytoprotective effect of reduced glutathione in hydrogen peroxide-induced endothelial cell injury",

abstract = "The kinetic effects of hydrogen peroxide (H2O2) on cultured endothelial cells isolated from bovine carotid artery were studied. The cytoprotective effects of glutathione (GSH) on H2O2-induced cell injury were also investigated. H2O2-induced a dose- and time-dependent cell injury in cultured endothelial cells. H2O2-induced cell injury was blocked by simultaneous treatment by catalase, but not by superoxide dismutase. H2O2 also induced endogenous PGI2 biosynthesis, and the maximum PGI2 production was reached after 1 h treatment. Stimulation of PGI2 production was parallel with arachidonate release from H2O2-treated cells. However the prostaglandin biosynthesis enzyme activity in cells was inhibited by H2O2 treatment. When the cells were treated with GSH, the intracellular GSH reached a plateau after 3 h treatment. Both H2O2-induced cell injury and PGI2 production were significantly inhibited by the 3 h pretreatment with GSH. The cytoprotective effect of GSH was completely inhibited by buthionine sulfoximine which is a specific inhibitor of γ-glutamylcysteine synthetase. The results indicate that the cytoprotective effect of GSH on H2O2-induced cell injury in cultured bovine carotid artery endothelial cells depends on the increase in intracellular GSH content.",

author = "Chen, {S. H.} and Wu, {H. L.} and Lin, {M. T.} and Jen, {C. J.} and Wing, {L. Y C} and Lei, {H. Y.} and Tsao, {C. J.} and Chang, {W. C.}",

year = "1992",

doi = "10.1016/0952-3278(92)90087-Y",

language = "English",

volume = "45",

pages = "299--305",

journal = "Prostaglandins Leukotrienes and Essential Fatty Acids",

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T1 - Cytoprotective effect of reduced glutathione in hydrogen peroxide-induced endothelial cell injury

AU - Chen, S. H.

AU - Wu, H. L.

AU - Lin, M. T.

AU - Jen, C. J.

AU - Wing, L. Y C

AU - Lei, H. Y.

AU - Tsao, C. J.

AU - Chang, W. C.

PY - 1992

Y1 - 1992

N2 - The kinetic effects of hydrogen peroxide (H2O2) on cultured endothelial cells isolated from bovine carotid artery were studied. The cytoprotective effects of glutathione (GSH) on H2O2-induced cell injury were also investigated. H2O2-induced a dose- and time-dependent cell injury in cultured endothelial cells. H2O2-induced cell injury was blocked by simultaneous treatment by catalase, but not by superoxide dismutase. H2O2 also induced endogenous PGI2 biosynthesis, and the maximum PGI2 production was reached after 1 h treatment. Stimulation of PGI2 production was parallel with arachidonate release from H2O2-treated cells. However the prostaglandin biosynthesis enzyme activity in cells was inhibited by H2O2 treatment. When the cells were treated with GSH, the intracellular GSH reached a plateau after 3 h treatment. Both H2O2-induced cell injury and PGI2 production were significantly inhibited by the 3 h pretreatment with GSH. The cytoprotective effect of GSH was completely inhibited by buthionine sulfoximine which is a specific inhibitor of γ-glutamylcysteine synthetase. The results indicate that the cytoprotective effect of GSH on H2O2-induced cell injury in cultured bovine carotid artery endothelial cells depends on the increase in intracellular GSH content.

AB - The kinetic effects of hydrogen peroxide (H2O2) on cultured endothelial cells isolated from bovine carotid artery were studied. The cytoprotective effects of glutathione (GSH) on H2O2-induced cell injury were also investigated. H2O2-induced a dose- and time-dependent cell injury in cultured endothelial cells. H2O2-induced cell injury was blocked by simultaneous treatment by catalase, but not by superoxide dismutase. H2O2 also induced endogenous PGI2 biosynthesis, and the maximum PGI2 production was reached after 1 h treatment. Stimulation of PGI2 production was parallel with arachidonate release from H2O2-treated cells. However the prostaglandin biosynthesis enzyme activity in cells was inhibited by H2O2 treatment. When the cells were treated with GSH, the intracellular GSH reached a plateau after 3 h treatment. Both H2O2-induced cell injury and PGI2 production were significantly inhibited by the 3 h pretreatment with GSH. The cytoprotective effect of GSH was completely inhibited by buthionine sulfoximine which is a specific inhibitor of γ-glutamylcysteine synthetase. The results indicate that the cytoprotective effect of GSH on H2O2-induced cell injury in cultured bovine carotid artery endothelial cells depends on the increase in intracellular GSH content.

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Cytoprotective effect of reduced glutathione in hydrogen peroxide-induced endothelial cell injury

Abstract

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UN SDGs

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