MECHANISMS of PATHOGENESIS in DRUG HEPATOTOXICITY PUTTING THE STRESS ON MITOCHONDRIA

被引：58

作者：

Jones, Dean P. ^{[2
]}

Lemasters, John J. ^{[3
]}

Han, Derick ^{[1
]}

Boelsterli, Urs A. ^{[4
]}

Kaplowitz, Neil ^{[1
]}

机构：

[1] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA

[2] Emory Univ, Dept Med, Rollins Res Ctr 4131, Atlanta, GA 30322 USA

[3] Med Univ S Carolina, Dept Pharmaceut Sci, Charleston, SC 29425 USA

[4] Univ Connecticut, Sch Pharm, Storrs, CT 06269 USA

来源：

MOLECULAR INTERVENTIONS | 2010年 / 10卷 / 02期

关键词：

INDUCED LIVER-INJURY; N-TERMINAL KINASE; GLYCOGEN-SYNTHASE KINASE-3-BETA; PERMEABILITY TRANSITION PORE; OXIDANT-INDUCED APOPTOSIS; HYDROGEN-PEROXIDE; OXIDATIVE STRESS; KEY ROLE; SUPEROXIDE-DISMUTASE; CULTURED-HEPATOCYTES;

D O I：

10.1124/mi.10.2.7

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Mitochondria play key roles in aerobic life and in cell death. Thus, interference of normal mitochondrial function impairs cellular energy and lipid metabolism and leads to the unleashing of mediators of cell death. The role of mitochondria in cell death due to drug hepatotoxicity has been receiving renewed attention and it is therefore timely to assess the current status of this area.

引用

页码：98 / 111

页数：14

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