HAAs are activation-dependent, heat-induced mutagenic agents predominantly present in foodstuffs containing nitrogenous and creatine components. The complex role that carcinogens play in the pathophysiology of cancer development remains obscure, but DNA damage remains pivotal to this process.
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Additionally, we allude to some of the cancer types where there is molecular epidemiological evidence that these agents are aetiological risk factors. This review predominantly concentrates on DNA damage induced by the following carcinogens: polycyclic aromatic hydrocarbons, heterocyclic aromatic amines, mycotoxins, ultraviolet light, ionising radiation, aristolochic acid, nitrosamines and particulate matter. Exposure to carcinogens is associated with various forms of DNA damage such as single-stand breaks, double-strand breaks, covalently bound chemical DNA adducts, oxidative-induced lesions and DNA–DNA or DNA–protein cross-links. One might reasonably surmise from this that carcinogens found in our environment or diet are culpable. That said, epidemiological studies of migrant populations from regions of low cancer risk to high cancer risk countries point to a role for environmental and/or lifestyle factors playing a pivotal part in cancer aetiology.
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DNA damage can arise from exposure to exogenous agents, but damage from endogenous processes is probably far more prevalent. Humans are variously and continuously exposed to a wide range of different DNA-damaging agents, some of which are classed as carcinogens.