Implication of mitochondria-derived ROS and cardiolipin peroxiclation in N-(4-hydroxyphenyl)retinamide-induced apoptosis

被引：83

作者：

Asumendi, A ^{[1
]}

Morales, MC ^{[1
]}

Alvarez, A ^{[1
]}

Aréchaga, J ^{[1
]}

Pérez-Yarza, H ^{[1
]}

机构：

[1] Univ Basque Country, Sch Med & Dent, Dept Cell Biol & Histol, Leioa 48940, Bizkaia, Spain

来源：

BRITISH JOURNAL OF CANCER | 2002年 / 86卷 / 12期

关键词：

N-(4-hydroxyphenyl)retinamide; apoptosis; reactive oxygen species; mitochondria; cardiolipin peroxidation; cytochrome c;

D O I：

10.1038/sj.bjc.6600356

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

We have studied the effect of N-(4-hydroxyphenyl)retinamide on either malignant human leukaemia cells or normal cells and investigated its mechanism of action. We demonstrate that 4HPR induces reactive oxygen species increase on mitochondria at a target between mitochondrial respiratory chain complex I and II. Such oxidative stress causes cardiolipin peroxidation which in turn allows cytochrome c release to cytosol, caspase-3 activation and therefore apoptotic consumption. Moreover, this apoptotic pathway seems to be bcl-2/bax independent and count only on malignant cells but not normal nor activated lymphocytes. (C) 2002 Cancer Research UK.

引用

页码：1951 / 1956

页数：6

共 20 条

[1]

DELIA D, 1993, CANCER RES, V53, P6036

[2] Role of antioxidants and intracellular free radicals in retinamide-induced cell death [J].