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Sci Total Environ. 2017 Aug 15;592:357-365. doi: 10.1016/j.scitotenv.2017.03.035. Epub 2017 Mar 17.

Bisphenol S exposure modulate macrophage phenotype as defined by cytokines profiling, global metabolomics and lipidomics analysis.

Author information

1
State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong, China; State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing, China.
2
State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong, China.
3
State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing, China.
4
State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong, China. Electronic address: zwcai@hkbu.edu.hk.

Abstract

As an important structural analogue of bisphenol A (BPA), bisphenol S (BPS) has been used as alternatives to BPA in industrialized production. However, the immunotoxicity of BPS remains poorly understood. As a critical model in inflammatory responses, macrophages are used to explore the immunotoxic potential and mechanisms of BPS at environmentally relevant concentrations in our study. Here, we are combining molecular toxicology and mass spectrometry (MS)-based global metabolomics and lipidomics study together to estimate the variation of cytokines profiling and metabolism characteristic following BPS exposure. Our results demonstrated that BPS exposure induced pro-inflammatory phenotype by activating the immuno-related cytokines which include TNF-α, IL-1β and IL-6, modulating metabolic pathways which include glycolytic, glutathione (GSH), sphingomyelin (SM)-ceramide (Cer), glycerophospholipids (GPs) and glycerolipids (GLs). These toxicological mechanisms are providing us with a deeper understanding of the critical role of metabolites and lipids reprogramming in immunotoxicity of BPS.

KEYWORDS:

Bisphenol S; Immunotoxicity; LC-MS/MS; Lipidomics; Metabolomics; Pro-inflammation

PMID:
28319722
DOI:
10.1016/j.scitotenv.2017.03.035
[Indexed for MEDLINE]

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