Department of Physiology, Medical College of Nanchang University, Nanchang 330006, China.
Department of Pathophysiology, Medical College of Nanchang University, Nanchang 330006, China.
Biomed Res Int. 2014;2014:409837. doi: 10.1155/2014/409837. Epub 2014 Mar 2.
Perfluorooctanoic acid (PFOA) is widely present in the environment and has been reported to induce hepatic toxicity in animals and humans. In this study, mice were orally administered different concentrations of PFOA (2.5, 5, or 10 mg/kg/day). Histological examination showed that the exposure to PFOA for 14 consecutive days led to serious hepatocellular injury and obvious inflammatory cell infiltration. In addition, malondialdehyde formation and hydrogen peroxide generation, indicators of oxidative stress, were significantly induced by PFOA treatment in the liver of mice. Furthermore, hepatic levels of interleukin-6, cyclooxygenase-2, and C-reactive protein, markers of inflammatory response, were markedly increased by exposure to PFOA in mice. These results demonstrated that PFOA-induced hepatic toxicity may be involved in oxidative stress and inflammatory response in mice.
全氟辛酸（PFOA）广泛存在于环境中，有报道称其可诱导动物和人类的肝毒性。在本研究中，小鼠经口给予不同浓度的 PFOA（2.5、5 或 10mg/kg/天）。组织学检查显示，连续 14 天暴露于 PFOA 可导致严重的肝细胞损伤和明显的炎性细胞浸润。此外，PFOA 处理可显著诱导小鼠肝脏中超氧化物歧化酶和过氧化氢的生成，这是氧化应激的指标。此外，PFOA 暴露可显著增加小鼠肝脏中白细胞介素-6、环氧合酶-2 和 C 反应蛋白等炎症反应标志物的水平。这些结果表明，PFOA 诱导的肝毒性可能涉及小鼠的氧化应激和炎症反应。
