Perfluorooctane sulfonate induces heart toxicity involving cardiac apoptosis and inflammation in rats

By Dongmin Xu, Li Li, Leilei Tang, Ming Guo, and Jie Yang
Exp Ther Med
December 6, 2021
DOI: 10.3892/etm.2021.10936

Perfluorooctane sulfonate (PFOS) is a persistent pollutant that exerts toxicity and induces cardiogenesis in humans and animals. Yet, the effect of PFOS exposure on cardiac toxicity in adult rats has, to our knowledge, not been reported and the mechanism still remains unknown. The present study aimed to investigate the toxicity of PFOS on rat hearts and any associated mechanisms. Rats were exposed to 0 (control), 1 and 10 mg/kg PFOS every other day for 14 days. Body weight and heart weight were recorded. The serum levels of lactic dehydrogenase (LDH), creatine kinase (CK), creatine kinase-isoenzyme-MB (CK-MB) and cardiac troponin-T (cTn-T) in heart tissues were measured using biochemical assays. TUNEL staining and western blotting were applied to analyze levels of apoptosis in rat hearts. Pathological assessment and immunohistochemistry analysis of heart tissues were used to evaluate the levels of PFOS-induced cardiotoxicity and inflammatory infiltration. PFOS exposure at the dosage of 10 mg/kg significantly increased the percentage of heart to body weight; however, it did not alter the body weight. At 10 mg/kg, PFOS significantly increased expression levels of myocardial injury markers, such as cTn-T, LDH, CK and CK-MB, while 1 mg/kg PFOS upregulated the expression level of cTn-T in rats. Notably, cardiac fibrosis and myocardiac hypertrophy appeared in the 10 mg/kg PFOS group. In addition, TUNEL-positive cells were significantly increased by exposure to 10 mg/kg PFOS in rat heart tissues. The protein expressions profiles of p53 and Bax were also significantly upregulated in the 10 mg/kg PFOS group. Inflammatory infiltration, detected by anaylzing expression levels of IL-1β and TNF-α, was significantly raised by 10 mg/kg PFOS exposure. In conclusion, these results demonstrated that 10 mg/kg PFOS-induced cardiac toxicity in rats, which was associated with an increase in apoptosis and the expression of proinflammatory cytokines.

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