پديد آورندگان :
Moghaddam-Jafari، Amir نويسنده Department of Toxicology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran Moghaddam-Jafari, Amir , Kazem Koohi، Mohammad نويسنده Department of Toxicology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran Kazem Koohi, Mohammad , Ghazi-Khansari، Mahmood نويسنده Department of Pharmacology, Tehran University of Medical Sciences, Tehran, Iran Ghazi-Khansari, Mahmood , Pasalar، Parvin نويسنده Department of Medical Biochemistry, Tehran University of Medical Sciences, Tehran, Iran Pasalar, Parvin
چكيده لاتين :
Background: The liver is the major target organ for aflatoxin B1 (AFB1). Ingestion of aflatoxin causes hepatotoxicty. In this study, captopril as new agent to help the hepatotoxicity induced by aflatoxin was suggested.
Materials and Methods: The isolated perfused rat liver (IPRL) was chosen for evaluating hepatic function. Sixteen rats were divided randomly into four experimental groups: control, captopril, AFB1 and AFB1 + captopril. The level of glutathione content and lipid peroxidation, as marker of oxidative stress and lactate dehydrogenase (LDH), alanine transaminase (ALT) and aspartate transaminase (AST) activities and pH of the perfusate medium were measured.
Results: There was a significant decrease in lipid peroxidation and same increase was observed in glutathione level. Treatment with captopril also modulated the enzymes activity and pH of perfusate.
Conclusion: This study showed that captopril protects the hepatotoxicty induced by AFB1. Therefore, this drug may provide an effective new strategy to reduce of aflatoxins toxicity.
