Journal
ENVIRONMENTAL RESEARCH
Volume 158, Issue -, Pages 490-498Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.envres.2017.07.005
Keywords
Bisphenol A; Inflammation; COX-2 expression; Epidemiology
Funding
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education, Science and Technology [2015M3C8A6A06014500]
- National Research Foundation of Korea [2015M3C8A6A06014500] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Bisphenol A (BPA) is a well-known endocrine-disrupting chemical, and it is one of the highest volume chemicals produced worldwide. Even though several in vivo and in vitro studies showed positive associations of BPA exposure with pro-inflammatory cytokines such as tumor necrosis factor-alpha and interleukin (IL)-6, the mechanism by which BPA induces inflammation is unclear. We investigated the mechanism by which BPA induces inflammation (expression of inflammation-related genes, changes in oxidative stress, and cell proliferation and migration) and evaluated the effect of BPA exposure on inflammation-related markers in epidemiologic studies using repeat urine and serum samples from elderly subjects. BPA induced COX-2 expression via nuclear translocation of NF-kappa B and activation of mitogen-activated protein kinase (MAPK) by phosphorylation of ERK1/2 and enhanced the migration of lung cancer A549 and breast cancer MDAMB-231 cells. In two epidemiologic studies, we detected associations of BPA with six inflammation -related markers (WBC, CRP, IL-10, ALT, AST, and gamma-GTP levels). Our findings probably suggest that BPA exposure induces inflammation and exacerbates tumorigenesis.
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