Enhanced hydroxychavicol-induced cytotoxic effects in glutathione-depleted HepG2 cells

被引：25

作者：

Chen, CL

Chi, CW

Liu, TY ^{[1
]}

机构：

[1] Natl Yang Ming Univ, Inst Pharmacol, Taipei 112, Taiwan

[2] Vet Gen Hosp, Dept Med Res & Educ, Taipei, Taiwan

来源：

CANCER LETTERS | 2000年 / 155卷 / 01期

关键词：

apoptosis; glutathione; hydroxychavicol; 8-hydroxy-2 '-deoxyguanosine;

D O I：

10.1016/S0304-3835(00)00404-3

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Hydroxychavicol (HC) is the major safrole urinary metabolite in rats and humans. The cytotoxic potential of HC in metabolically competent cells has yet to be studied. HC alone was slightly toxic to HepG2 cells. However, the cytotoxicity increased significantly (P < 0.05) when HepG2 cells were pretreated with buthionine sulfoximine (BSO), suggesting that endogenous glutathione participates in HC-induced cytotoxicity. Addition of catalase or N-acetylcysteine prevented the BSO plus HC-mediated cytotoxicity. HC also increased 8-hydroxy-2'-deoxyguanosine formation and apoptosis in BSO-pretreated HepG2 cells and this increase could also be suppressed by catalase. These data suggest that BSO pretreatment enhanced HC-induced cytotoxic effects in HepG2 cells, which are related to oxidative DNA damage. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：29 / 35

页数：7

共 24 条

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