Potential molecular mechanisms for combined toxicity of arsenic and alcohol

被引：23

作者：

Bao, Lingzhi ^{[1
]}

Shi, Honglian ^{[1
]}

机构：

[1] Univ Kansas, Dept Pharmacol & Toxicol, Sch Pharm, Lawrence, KS 66045 USA

来源：

JOURNAL OF INORGANIC BIOCHEMISTRY | 2010年 / 104卷 / 12期

关键词：

Arsenic; Alcohol; Co-exposure; Reactive oxygen species; Toxicity; MITOCHONDRIAL PERMEABILITY TRANSITION; INDUCED OXIDATIVE STRESS; HAMSTER OVARY CELLS; REACTIVE OXYGEN; DNA-DAMAGE; UROTHELIAL CARCINOMA; ENDOTHELIAL-CELLS; RAT HEPATOCYTES; CARDIOVASCULAR-DISEASES; N-ACETYLCYSTEINE;

D O I：

10.1016/j.jinorgbio.2010.08.005

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：

Arsenic is a ubiquitous environmental factor that has been identified as a risk factor for a wide range of human diseases. Alcohol is clearly a toxic substance when consumed in excess. Alcohol abuse results in a variety of pathological effects, including damages to liver, heart, and brain, as well as other organs, and is associated with an increased risk of certain types of cancers. In history, arsenic-contaminated beers caused severe diseases. There are populations who are exposed to relatively high levels of arsenic in their drinking water and consume alcohol at the same time. In this focused review, we aim to discuss important molecular mechanisms responsible for arsenic toxicity and potential combined toxic effects of alcohol and arsenic. (C) 2010 Elsevier Inc. All rights reserved.

引用

页码：1229 / 1233

页数：5

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