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化学致癌作用中的氧化应激和氧化损伤。

Oxidative stress and oxidative damage in chemical carcinogenesis.

机构信息

Department of Environmental Health, Indiana University, 1025 East 7th St., Bloomington, Indiana 47405, USA.

出版信息

Toxicol Appl Pharmacol. 2011 Jul 15;254(2):86-99. doi: 10.1016/j.taap.2009.11.028. Epub 2011 Feb 4.

DOI:10.1016/j.taap.2009.11.028
PMID:21296097
Abstract

Reactive oxygen species (ROS) are induced through a variety of endogenous and exogenous sources. Overwhelming of antioxidant and DNA repair mechanisms in the cell by ROS may result in oxidative stress and oxidative damage to the cell. This resulting oxidative stress can damage critical cellular macromolecules and/or modulate gene expression pathways. Cancer induction by chemical and physical agents involves a multi-step process. This process includes multiple molecular and cellular events to transform a normal cell to a malignant neoplastic cell. Oxidative damage resulting from ROS generation can participate in all stages of the cancer process. An association of ROS generation and human cancer induction has been shown. It appears that oxidative stress may both cause as well as modify the cancer process. Recently association between polymorphisms in oxidative DNA repair genes and antioxidant genes (single nucleotide polymorphisms) and human cancer susceptibility has been shown.

摘要

活性氧(ROS)可由多种内源性和外源性物质诱导产生。ROS 会使细胞中的抗氧化和 DNA 修复机制不堪重负,从而导致氧化应激和细胞氧化损伤。这种氧化应激会损害关键的细胞大分子,并/或调节基因表达途径。化学和物理因子诱导癌症的发生涉及多步过程。该过程包括多个分子和细胞事件,使正常细胞转化为恶性肿瘤细胞。ROS 产生导致的氧化损伤可参与癌症过程的所有阶段。ROS 的产生与人类癌症的发生之间存在关联。氧化应激似乎既可以引发癌症,也可以改变癌症进程。最近,氧化 DNA 修复基因和抗氧化基因(单核苷酸多态性)中的多态性与人类癌症易感性之间的关联已被证实。

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