Bisphenol A as epigenetic modulator: setting the stage for carcinogenesis?

被引:34
作者
Ferreira, Luciana L. [1 ,2 ]
Couto, Renata [1 ,3 ]
Oliveira, Paulo J. [1 ]
机构
[1] Univ Coimbra, CNC Ctr Neurosci & Cell Biol, Coimbra, Portugal
[2] Univ Coimbra, Doctoral Programme Med Biochem & Biophys, Coimbra, Portugal
[3] Univ Coimbra, Dept Life Sci, Coimbra, Portugal
关键词
Bisphenol A; cancer; endocrine-disrupting chemicals; epigenetics; epigenotoxicity; ENDOCRINE DISRUPTING CHEMICALS; STRAND BREAK REPAIR; DNA-DAMAGE; IN-VITRO; ENVIRONMENTAL ESTROGENS; EXPOSURE; CELLS; EXPRESSION; CANCER; DIETHYLSTILBESTROL;
D O I
10.1111/eci.12362
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BackgroundBisphenol A (BPA) is one of the most widely produced chemicals worldwide and is often used in the production of food and beverage containers. As a result of BPA contact with food, drink and toiletries, its ingestion and absorption by humans has been growing. The industrialization and modern lifestyles brought a constant exposure to several health-disturbing compounds and ushered a new era of chronic diseases. The endocrine disruptor potential of BPA is well known, but the research around its epigenotoxic effects raised further concerns whether chronic exposure to BPA can contribute to chronic human illness, including cancer in hormone-sensitive organs. Materials and methodsFocusing on computerized databases, we reviewed original and review articles which elucidate and link some of the information already available about BPA and related epigenetic alterations. ResultsA number of studies indicate that short-term administration of low or high-doses of BPA may be associated with an increased risk of epigenetic modifications, increasing the risk for carcinogenesis. However, it is clear that more studies considering real daily exposures are essential to define a real tolerable daily intake and to tighten\xA0up\xA0manufactory regulations. ConclusionIn this review, we highlight some evidences suggesting a relationship between BPA exposure, genotoxic activity and epigenetic modifications, which may prime for carcinogenesis.
引用
收藏
页码:32 / 36
页数:5
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