N-acetyl cysteine abates hepatorenal toxicities induced by perfluorooctanoic acid exposure in male rats

•Perfluorooctanoic acid (PFOA) effect on rats’ hepatorenal function was investigated.•PFOA-mediated tissue injury was abated by N-acetylcysteine (NAC) co-treatment.•NAC abrogated the hepatorenal oxidative injury induced by PFOA co-exposure.•NAC suppressed induction of inflammation incumbent on PFOA dosing in rats.•PFOA-induced damage significantly reduces in the NAC co-treated groups. Ingestion of perfluorooctanoic acid (PFOA) elicits toxicities in the hepatorenal system. We investigated the effect of PFOA and N-acetylcysteine (NAC) on the hepatorenal function of rats treated thus: control, PFOA (5 mg/kg), NAC (50 mg/kg), PFOA + NAC (5 and 25 mg/kg), and PFOA + NAC (5 and 50 mg/kg). We observed that NAC significantly (p < 0.05) reduced PFOA-induced increase in hepatic and renal function biomarkers of toxicities relative to PFOA alone and alleviated (p < 0.05) decreases in antioxidant status. Increases in oxidative stress and lipid peroxidation in PFOA-treated rats were reverted to normal by NAC and abated increased pro-inflammatory mediators, and decreased anti-inflammatory cytokine both in the hepatorenal system PFOA treated rats. Histology of the kidney and liver indicated that NAC, abated the severity of PFOA-induced damage significantly. Our findings affirm further that oxido-inflammatory mediators involved in PFOA-mediated toxicity can be effectively blocked by NAC through its antioxidant activity.