Özet:
Background and Aims. Despite it being a highly potent antineoplastic drug, cisplatin has
important toxic adverse effects limiting its use such as nephrotoxicity, neurotoxicity and
ototoxicity. It is thought that cisplatin-induced hepatotoxicity is caused by oxidative
stress resulting from increased reactive oxygen species (ROS). Apocynin (APO) exerts
its antioxidant effect by reducing ROS production via inhibition of NADPH oxidase.
The present study intended to demonstrate effects of cisplatin on hepatic pro-oxidant/
antioxidant systems and to investigate protective effects of APO against cisplatininduced
hepatotoxicity.
Methods. Rats were randomly assigned into four groups (n 5 8 each): a) control group;
b) single dose of cisplatin (5 mg/kg); c) APO group (20 mg/kg on three consecutive days;
i.p.); and d) APO plus cisplatin group. Liver tissue was assessed in all groups by
biochemical and histopathological means. Also, serum alanine transaminase (ALT),
aspartate transaminase (AST) and alkaline phosphatase levels were studied in all groups.
Results. When cisplatin group was compared to controls, it was seen that lipid peroxidation
product, total oxidant status and ALT levels were markedly increased, whereas superoxide
dismutase and glutathione peroxidase levels were overtly decreased. APO
therapy markedly prevented cisplatin-induced harmful changes in liver. Our histopathological
findings such as central vein dilatation, perivenuler and periportal sinusoidal dilatation,
parenchymal inflammation, vacuolar changes in hepatocytes, biliary duct
proliferation and caspase-3 positive hepatocytes were in accordance with the biochemical
changes.
Conclusion. In light of these results, it is our thought that APO has a protective role
against cisplatin-induced hepatotoxicity at both biochemical and histopathological
levels.