Assessment of cardiotoxicity induced by PFOS exposure and mechanism research via untarget metabolomics

Abstract

Perfluorooctane sulfonate (PFOS), widely used in various industrial and commercial materials, can accumulate in the human body due to its high environmental stability, and thus potentially has cardiotoxicity. We assess cardiotoxicity through rat exposure to PFOS by intraperitoneal injection. Untargeted metabolomic analysis was used to explore the potential cardiotoxicity mechanism of PFOS. In vivo, PFOS exposure increases pro-inflammatory factors TNF-α and IL-1β and decreases anti-inflammatory factors IL-10 and TGF-β. PFOS exposure causes pathological changes in cardiac tissue and increases cardiac injury markers brain natriuretic peptide (BNP), lactate dehydrogenase (LDH), C-reactive protein (CRP) in serum and triglyceride (TG), total cholesterol (TC) and ox-LDL in plasma. Increased expression of plasminogen activator inhibitor-1 (PAI-1) and CD36 indicates that PFOS exacerbates cardiac fibrosis. Untargeted metabolites analysis revealed 414 small molecule metabolites and 33 metabolites that differed after PFOS exposure, and identified 3 potential metabolic pathways. In conclusion, our study shows the inflammatory reactions involved in PFOS cardiotoxicity, and identifies potential pathways and differential metabolites involved in PFOS toxicity.

Keywords:

• PFOS
• inflammation
• cardiotoxicity
• untarget metabolism
• fibrosis

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

All data will be available from the corresponding authors upon reasonable request.

Additional information

Funding

This work was supported by Hangzhou Science and Technology Plan Guidance Project [20220919Y087].