Postnatal exposure to Bisphenol S induces liver injury in mice: Possible implication of PPARγ receptor

Author:

Mornagui Bessem1ORCID,Rezg Raja2ORCID,Neffati Fadoua3,Najjar Mohamed Fadhel34,Rejeb Ahmed5

Affiliation:

1. University of Gabes, Faculty of Sciences of Gabes, LR-18ES36, Gabes, Tunisia

2. University of Monastir, ISBM, Biolival LR-14ES06, Monastir, Tunisia

3. University of Monastir, University Hospital of Fattouma Bourguiba, Laboratory of Biochemistry-Toxicology, Monastir, Tunisia

4. University of Monastir, Faculty of Pharmacy of Monastir, Monastir, Tunisia

5. University of Manouba, National School of Veterinary Medicine of Sidi Thabet, Laboratory of Pathological Anatomy, Manouba 1144, Tunisia.

Abstract

There is considerable evidence that Bisphenol S (BPS) induces various toxicological effects and is an industrial health issue. However, little data are available on the in vivo effects of BPS on the liver, a major target of drug toxicity. In this study, we evaluated the potential harmfulness of low levels of BPS in the liver of male mice. Also, we investigated the interaction between BPS and peroxisome proliferator-activated receptor-gamma (PPARγ) by computational docking approach. PPARγ is a member of the superfamily of nuclear hormone receptors. It acts as a transcription factor and regulates the genes involved in lipid and glucose metabolism and in inflammation and necrosis. Mice were exposed to BPS, in drinking water at 25, 50, and 100 μg/kg for 10 weeks. The protocol was started after weaning. At the time of sacrifice, blood samples were collected for a biochemical analysis, followed by liver tissue collection for histopathological study. Results showed that BPS-induced hypertriglyceridemia, increased liver injury markers, and initiated histopathological changes, including inflammatory cell infiltration, hepatocellular necrosis, and steatosis. BPS did not affect glycated hemoglobin (HbA1C). Interestingly, data showed that BPS could interact with the PPARγ ligand-binding pocket by hydrogen bonds with Asn 219, Cys 276, Ser 280, and Thr 283. We suggest that PPARγ is among the targets of BPS and could play a key role in the cascade reaction of BPS-induced liver disruption. These findings support the hypothesis that the post-weaning period is sensitive to low-dose BPS exposure that can lead to dyslipidemia signature later in life.

Funder

Tunisian Ministry of Higher Education and Scientific Research

Publisher

SAGE Publications

Subject

Health, Toxicology and Mutagenesis,Public Health, Environmental and Occupational Health,Toxicology

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