作者: Akram Jamshidzadeh , Hossein Niknahad , Reza Heidari , Maryam Azadbakht , Forouzan Khodaei
DOI: 10.15171/PS.2017.15
关键词:
摘要: Background: Propylthiouracil (PTU) administration is associated with several cases of hepatotoxicity, especially in children. The mechanism(s) PTU-induced hepatotoxicity obscure. In the current study, we aimed to assess effect PTU on hepatocytes mitochondria different experimental models. Methods: Mice were treated (10, 20, 40, 80, and 100 mg/kg, i.p) then, liver mitochondria were isolated evaluated. Moreover, liver were isolated from normal mice incubated increasing concentrations PTU (10 µM-1 mM). Mitochondrial dehydrogenases activity, mitochondrial membrane potential, swelling, adenosine triphosphate (ATP) content monitored. Results: PTU hepatotoxicity was biochemically evident by increased serum biomarkers of injury. also caused a decrease in swelling, depleted ATP, caused mitochondrial depolarization both vitro vivo. Conclusion: Our data suggest dysfunction as mechanism for PTU-induced hepatotoxicity.