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Environ Res. 2017 Oct;158:490-498. doi: 10.1016/j.envres.2017.07.005. Epub 2017 Jul 11.

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

Author information

1
Department of Integrative Bioscience and Biotechnology, College of Life Science, Sejong University, Kwangjin-gu, Seoul 05006, Republic of Korea.
2
Department of Life Science, Hanyang University, Seoul 04763, Republic of Korea.
3
Department of Preventive Medicine, Seoul National University College of Medicine, Seoul 110-799, Republic of Korea.
4
Department of Integrative Bioscience and Biotechnology, College of Life Science, Sejong University, Kwangjin-gu, Seoul 05006, Republic of Korea. Electronic address: jhkim777@sejong.ac.kr.
5
Department of Integrative Bioscience and Biotechnology, College of Life Science, Sejong University, Kwangjin-gu, Seoul 05006, Republic of Korea. Electronic address: yjlee@sejong.ac.kr.

Abstract

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-α 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-κB 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 γ-GTP levels). Our findings probably suggest that BPA exposure induces inflammation and exacerbates tumorigenesis.

KEYWORDS:

Bisphenol A; COX-2 expression; Epidemiology; Inflammation

PMID:
28709031
DOI:
10.1016/j.envres.2017.07.005
[Indexed for MEDLINE]

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