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.

摄入全氟辛酸 (PFOA) 会引起肝肾系统毒性。我们研究了 PFOA 和N-乙酰半胱氨酸 (NAC) 对如此处理的大鼠肝肾功能的影响：对照、PFOA (5 mg/kg)、NAC (50 mg/kg)、PFOA + NAC (5 和 25 mg/kg) ）和 PFOA + NAC（5 和 50 毫克/千克）。我们观察到，与单独使用 PFOA 相比，NAC 显​​着 ( p < 0.05 ) 降低了 PFOA 诱导的肝肾功能生物标志物的毒性增加，并缓解(p < 0.05)抗氧化状态的降低。 PFOA 治疗大鼠的氧化应激和脂质过氧化增加可通过 NAC 恢复正常，并减少 PFOA 治疗大鼠肝肾系统中促炎介质的增加，并减少抗炎细胞因子。肾脏和肝脏的组织学表明 NAC 显​​着减轻了 PFOA 引起的损伤的严重程度。我们的研究结果进一步证实，NAC 通过其抗氧化活性可以有效地阻断参与 PFOA 介导的毒性的氧化炎症介质。