Silencing of cytosolic NADP+-dependent isocitrate dehydrogenase gene enhances ethanol-induced toxicity in HepG2 cells

被引：4
|
作者：
Yang, Eun Sun [1 ]
Lee, Su-Min [1 ]
Park, Jeen-Woo [1 ]
机构：
[1] Kyungpook Natl Univ, Sch Life Sci & Biotechnol, Coll Nat Sci, Taegu 702701, South Korea
来源：
ARCHIVES OF PHARMACAL RESEARCH | 2010年 / 33卷 / 07期
关键词：
Ethanol; Antioxidant enzyme; Reactive oxygen species; siRNA; ALCOHOLIC LIVER-DISEASE; LIPID-PEROXIDATION; OXIDATIVE STRESS; SUPEROXIDE-DISMUTASE; MOLECULAR CHAPERONES; RAT-LIVER; SH-GROUPS; INJURY; PATHOGENESIS; PROTEINS;
D O I：
10.1007/s12272-010-0713-4
中图分类号：
R914 [药物化学];
学科分类号：
100701 ;
摘要：
It has been shown that acute and chronic alcohol administrations increase the production of reactive oxygen species, lower cellular antioxidant levels and enhance oxidative stress in many tissues. We recently reported that cytosolic NADP(+)-dependent isocitrate dehydrogenase (IDPc) functions as an antioxidant enzyme by supplying NADPH to the cytosol. Upon exposure to ethanol, IDPc was susceptible to the loss of its enzyme activity in HepG2 cells. Transfection of HepG2 cells with an IDPc small interfering RNA noticeably downregulated IDPc and enhanced the cells' vulnerability to ethanol-induced cytotoxicity. Our results suggest that suppressing the expression of IDPc enhances ethanol-induced toxicity in HepG2 cells by further disruption of the cellular redox status.
引用
收藏
页码：1065 / 1071
页数：7
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