Abstract Title:

Mechanism investigation on Bisphenol S-induced oxidative stress and inflammation in murine RAW264.7 cells: The role of NLRP3 inflammasome, TLR4, Nrf2 and MAPK.

Abstract Source:

J Hazard Mater. 2020 07 15 ;394:122549. Epub 2020 Apr 10. PMID: 32283380

Abstract Author(s):

Chunfeng Xie, Miaomiao Ge, Jianliang Jin, Haie Xu, Li Mao, Shanshan Geng, Jieshu Wu, Jianyun Zhu, Xiaoting Li, Caiyun Zhong

Article Affiliation:

Chunfeng Xie


Bisphenol S is considered as a safer alternative to bisphenol A. In the present study, we used murine macrophages to investigate the effects of BPS exposure on oxidative stress and inflammatory response as well as the underlying mechanism. Cells were exposed to BPS at various concentrations for short period of times. Results showed that 10M BPS triggered oxidative stress by increasing ROS/RNS production, increased the levels of oxidant enzyme NOX1/2, and decreased the levels of antioxidant enzymes SOD1/2, CAT and GSH-Px. 10M BPS exposure significantly induced the production of proinflammatory mediators. Activation of the NLRP3 inflammasome, TLR4, and MAPK pathways was involved in this process. Furthermore, we illustrated that NAC pretreatment diminished these effects triggered by BPS exposure. Collectively, our data suggested that BPS at a dose relevant to human serum concentration induced oxidative stress and inflammatory response in macrophages. These novel findings shed light on the concerns regarding the potential adverse effects of BPS exposure that requires further careful attention.

Study Type : In Vitro Study

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