A Short Review on Carcinogenicity

Dhananjay D. Chaudhari, Karishma. P. Bhadane, Priyanka. V. Pawar
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Abstract

Humans are exposed to a variety of different and persistent DNA-damaging agents, some of which have been identified as carcinogens. DNA damage can occur from exposure to exogenous agents, but damage from endogenous processes is more common. That is, epidemiological studies of migrant populations from low-cancer-risk areas to high-cancer-incidence countries suggest the role of environmental factors and/or lifestyle as important players in the etiology of cancer. As a result, it can be assumed that carcinogens found in the environment or our diet are to blame. Carcinogen exposure is associated with various forms of DNA damage, including single-strand breaks, double-strand breaks, chemical DNA cross-links, oxidative stress, and DNA-DNA or DNA-protein breaks. This review focuses on DNA damage caused by the following carcinogens: polycyclic aromatic hydrocarbons, heterocyclic aromatic amines, mycotoxins, ultraviolet light, ionizing radiation, aristolochic acid, nitrosamines, and particulate matter. In addition, we discuss several cancers for which molecular epidemiological evidence suggests that these agents are etiological risk factors. The complex role that carcinogens play in the pathophysiology of cancer development remains unclear, but DNA damage remains central to this process.
致癌性研究综述
人类暴露于各种不同的和持久的dna损伤剂,其中一些已被确定为致癌物。DNA损伤可由暴露于外源性因素引起,但内源性过程的损伤更为常见。也就是说,从低癌症风险地区到高癌症发病率国家的移民人口的流行病学研究表明,环境因素和/或生活方式在癌症病因学中起着重要作用。因此,可以假设环境中发现的致癌物或我们的饮食是罪魁祸首。致癌物质暴露与多种形式的DNA损伤有关,包括单链断裂、双链断裂、化学DNA交联、氧化应激以及DNA-DNA或DNA-蛋白质断裂。本文综述了多环芳烃、杂环芳烃胺、真菌毒素、紫外线、电离辐射、马兜铃酸、亚硝胺和颗粒物等致癌物引起的DNA损伤。此外,我们讨论了分子流行病学证据表明这些药物是病因危险因素的几种癌症。致癌物在癌症发展的病理生理中所起的复杂作用尚不清楚,但DNA损伤仍然是这一过程的核心。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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