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Mutagenicity and carcinogenicity

Authors
Kim, H.S.[Kim, H.S.]Lee, B.-M.[Lee, B.-M.]
Issue Date
2017
Publisher
Elsevier
Keywords
Cancer; Endocrine disruptor; Epigenetic; Genotoxic; Reproductive; Transgeneration
Citation
Reproductive and Developmental Toxicology, pp.1123 - 1138
Indexed
SCOPUS
Journal Title
Reproductive and Developmental Toxicology
Start Page
1123
End Page
1138
URI
https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/101544
DOI
10.1016/B978-0-12-804239-7.00060-3
ISSN
0000-0000
Abstract
Endocrine disruptors are chemicals that produce various toxicities such as developmental or reproductive toxicity, carcinogenicity, mutagenicity, immunotoxicity, and neurotoxicity (Choi et al., 2004). Mechanisms of carcinogenesis caused by exposure to endocrine disruptors may be associated with free radical generation and biomolecule (e.g., DNA, protein, lipid) damage after the dysregulation of hormones such as estrogen, testosterone, thyroid, and insulin. The hormonal effect on carcinogenesis is receptor dependent or receptor independent, and there is often cross-talk between hormones and complex signaling cascades may also be involved. During multistage carcinogenesis {i.e., initiation, promotion [stage I (reversible), stage II (irreversible)], progression}, genotoxic and epigenetic events are critically associated, which may lead to mutation and cancer. Although genotoxic events are fundamentally the limiting step in carcinogenesis and reproductive disorders, the transgenerational epigenetic role of carcinogens could also be important. Given the unavoidable human exposure to endocrine disruptors or carcinogens, the application of a chemopreventive strategy that either blocks or retards the process of carcinogenesis might be helpful for public health. © 2017 Elsevier Inc. All rights reserved.
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