Bisphenol A induces COX-2 through the mitogen-activated protein kinase pathway and is associated with levels of inflammation-related markers in elderly populations

作者：Song Heewon; Park Joonwoo; Bui Phuong T C; Choi KeunOh; Gye Myung Chan; Hong Yun Chul; Kim Jin Hee^*; Lee Young Joo^*

来源：Environmental Research, 2017, 158: 490-498.

DOI：10.1016/j.envres.2017.07.005

• Bisphenol A
• Inflammation
• COX-2 expression
• Epidemiology

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.

• 出版日期2017-10