Reactive oxygen species generated by cyanide mediate toxicity in rat pheochromocytoma cells

被引：25

作者：

Kanthasamy, AG ^{[1
]}

Ardelt, B ^{[1
]}

Malave, A ^{[1
]}

Mills, EM ^{[1
]}

Powley, TL ^{[1
]}

Borowitz, JL ^{[1
]}

Isom, GE ^{[1
]}

机构：

[1] PURDUE UNIV, DEPT MED CHEM & MOL PHARMACOL, LAB NEUROTOXICOL, W LAFAYETTE, IN 47907 USA

来源：

TOXICOLOGY LETTERS | 1997年 / 93卷 / 01期

关键词：

lipid peroxidation; catalase; malondialdehyde; dichlorofluorescin; ascorbic acid; phospholipase A(2);

D O I：

10.1016/S0378-4274(97)00068-4

中图分类号：

R99 [毒物学（毒理学）];

学科分类号：

100405 ;

摘要：

Peroxide formation has been implicated in impairment of motor function by cyanide which occurs in both animals and man. The present study employs the neuronal model, rat pheochromocytoma (PC12) cells to evaluate peroxidation as a toxic mechanism of cyanide. Confocal imaging shows that peroxides form within a few seconds in cell cytoplasm after cyanide exposure and continue to accumulate over a period of several minutes. Peroxide generation by cyanide is decreased to about 50% by phospholipase A(2) inhibitors indicating involvement of arachidonic acid in the oxidative process. Also antioxidant defense enzymes (CuZn superoxide dismutase and especially catalase) in PC12 cells are inhibited by cyanide. It appears that peroxide accumulation after cyanide treatment involves both inhibition of breakdown and increased production. Furthermore, both peroxide accumulation and cell death induced by cyanide in PC12 cells are blocked by an antioxidant (ascorbate). These data support the hypothesis that the cytotoxic action of cyanide is related in part to an oxidative process. (C) 1997 Elsevier Science Ireland Ltd.

引用

页码：47 / 54

页数：8

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