Akpinar, MBErdogan, HSahin, SUcar, FIlhan, A2024-08-042024-08-0420050048-35751095-9939https://doi.org/10.1016/j.pestbp.2005.03.003https://hdl.handle.net/11616/93972Rotenone, an insecticide, causes toxicity through inhibition of mitochondrial electron transport chain at complex I and oxidative injury to the tissues. The aim of the present study was to determine in vivo effects of rotenone on myocardium and cardio-protective effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, against rotenone toxicity in rats. The rats were divided into three groups: untreated control, rotenone (2.5 mg/kg/day for 60 days, i.p.) and rotenone + CAPE groups. CAPE was administrated i.p. 10 ltmol/kg/day for 62 days started two days before first dose rotenone injection. The malondialdehyde, nitric oxide levels and xanthine oxidase activity of rotenone group was significantly higher than control and rotenone + CAPE groups (to < 0.05). However, catalase activity in the rotenone group was decreased in comparison with the other groups (p < 0.05). The superoxide dismutase activity of rotenone group was insignificantly decreased compared to the others. In conclusion, rotenone caused lipid peroxidation in myocardial tissue and CAPE treatment prevented this rotenone-induced lipid peroxiclation in rats. CAPE might be a cardio-protective agent against myocardial toxicities. (c) 2005 Elsevier Inc. All rights reserved.eninfo:eu-repo/semantics/closedAccessrotenoneheartoxidants/antioxidantslipidperoxidationnitric oxideCAPEArticle82323323910.1016/j.pestbp.2005.03.0032-s2.0-20644448596Q1WOS:000230049000007Q2