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N-acetyl cysteine abates hepatorenal toxicities induced by perfluorooctanoic acid exposure in male rats
Affiliation:1. CRMB Laboratory, Biochemistry Department, Faculty of Basic Medical Sciences, College of Medicine, University of Ibadan, Ibadan, 200004, Nigeria;2. School of Biochemistry and Chemistry, and Parker H. Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, GA, 30332-0400, USA;1. Atherosclerosis Research Center, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing 210029, People’s Republic of China;2. Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing 210029, People’s Republic of China;1. Department of Pediatrics, Peking University First Hospital, No.1 Xi''an Men Street, West District, Beijing, 100034, China;2. Department of Pediatrics, The Second Affiliated Hospital and Yuying Children''s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325027, China;3. Guangdong Provincial Key Laboratory of Bioengineering Medicine, Department of Cell Biology, Jinan University, Guangzhou, 510632, China;4. Department of Anesthesiology, Center of Scientific Research, The Second Affiliated Hospital and Yuying Children''s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325027, China;1. College of Life and Environmental Sciences, Hangzhou Normal University, Xuelin Road 16#, Xiasha Gaojiao Dongqu, Hangzhou, Zhejiang Province 310036, China;2. Guangzhou Key Laboratory of Environmental Exposure and Health, School of Environment, Jinan University, Guangzhou 510632, China;3. Key Laboratory of Hangzhou City for Ecosystem Protection and Restoration, Hangzhou Normal University, Hangzhou, Zhejiang Province 310036, China;1. State Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, 214122, PR China;2. School of Food Science and Technology, Jiangnan University, Wuxi, 214122, PR China;3. Department of Gastroenterology, Affiliated Hospital of Jiangnan University, Wuxi, 214122, PR China;4. (Yangzhou) Institute of Food Biotechnology, Jiangnan University, Yangzhou, 225004, PR China;5. National Engineering Research Center for Functional Food, Jiangnan University, Wuxi, 214122, PR China;6. Wuxi Translational Medicine Research Center and Jiangsu Translational Medicine Research Institute Wuxi Branch, Wuxi, 214122, PR China;7. International Joint Research Laboratory for Probiotics, Jiangnan University, Wuxi, 214122, PR China;8. Beijing Innovation Centre of Food Nutrition and Human Health, Beijing Technology and Business University (BTBU), Beijing, 100048, PR China;1. College of Life and Environmental Sciences, Hangzhou Normal University, Xuelin Road 16#, Xiasha Gaojiao Dongqu, Hangzhou, Zhejiang Province, 310036, China;2. Guangzhou Key Laboratory of Environmental Exposure and Health, School of Environment, Jinan University, Guangzhou, 510632, China;3. Key Laboratory of Hangzhou City for Ecosystem Protection and Restoration, Hangzhou Normal University, Hangzhou, 310036, China;1. State Key Laboratory of Reproductive Medicine, School of Public Health, Nanjing Medical University, Nanjing, China;2. Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, Nanjing Medical University, Nanjing, China;3. Center of Gallbladder Disease, Shanghai East Hospital, Institute of Gallstone Disease, Tongji University School of Medicine, Shanghai, China;4. Department of Maternal, Child and Adolescent Health, School of Public Health, Nanjing Medical University, Nanjing, China;5. School of Instrument Science and Engineering, Southeast University, Nanjing, 210096, PR China
Abstract: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.
Keywords:Perfluorooctanoic acid  Hepatorenal toxicity  Oxido-inflammatory stress  Chemoprevention
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