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.
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