OXIDATIVE MECHANISMS IN CARCINOGENESIS
OXIDATIVE MECHANISMS IN CARCINOGENESIS
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DOI：
10.1093/oxfordjournals.bmb.a072628
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发表时间：
1993-07-01
影响因子：
6.7
通讯作者：
KENSLER, TW
中科院分区：
文献类型：
--
作者：
GUYTON, KZ;KENSLER, TW
人类和动物的癌症是一个多步骤的疾病过程。在这个过程中，单个细胞可以从正常组织发展成恶性肿瘤，最终摧毁生物体。癌症发展过程中发生的一系列复杂的细胞和分子变化可以由多种内源性和环境刺激介导。活性氧和其他自由基早已被认为是致突变的;此外，这些药物最近出现作为其他表型和基因型变化的介导剂，导致从突变到瘤形成。自由基的产生普遍存在于所有呼吸生物体中，并且在许多疾病状态下，通过致癌物暴露和压力条件下增强。因此，自由基可能广泛地促进人类癌症的发展。本文综述了自由基参与致癌过程的分子机制。
Cancer in humans and animals is a multistep disease process. In this process, a single cell can develop from an otherwise normal tissue into a malignancy that can eventually destroy the organism. The complex series of cellular and molecular changes that occur through the development of cancers can be mediated by a diversity of endogenous and environmental stimuli. Active oxygen species and other free radicals have long been known to be mutagenic; further, these agents have more recently emerged as mediators of the other phenotypic and genotypic changes that lead from mutation to neoplasia. Free radical production is ubiquitous in all respiring organisms, and is enhanced in many disease states, by carcinogen exposure, and under conditions of stress. Free radicals may therefore contribute widely to cancer development in humans. This review explores the molecular mechanisms through which free radicals can participate in the carcinogenic process.