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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