Akademik Veri Yönetim Sistemi
Pesticide Biochemistry and Physiology, cilt.97, sa.3, ss.249-255, 2010 (SCI-Expanded)
Recent several studies have reported that oxidative stress could be an important component of the mechanism of cardiotoxicity due to organophosphate-induced toxicity. The aim of this study is to evaluate the oxidative and antioxidative parameters in cardiac toxicity of organophosphate poisoning, and determine the effects of atropine and pralidoxime on this parameters. The experimental groups were randomly divided into five groups as control (corn oil), dichlorvos (30 mg/kg), atropine (10 mg/kg), pralidoxime (40 mg/kg), and atropine (10 mg/kg) + pralidoxime (40 mg/kg) groups. Serum cholinesterase levels were suppressed with dichlorvos, and these reductions were inhibited with atropine and/or pralidoxime pretreatment. Serum, but not cardiac, total free sulfhydryl groups and paraoxonase activities were significantly increased in the pralidoxime group when compared to the control group. Serum arylesterase activities were elevated in the dichlorvos, atropine, pralidoxime, and atropine + pralidoxime groups when compared to the control group (P < 0.05). Total oxidant status, oxidative stress index, malondialdehyde and catalase activities in serum and cardiac tissues were not markedly different between the groups. No significant changes were also observed with cardiac myeloperoxidase and serum ceruloplasmin activities. In conclusion, these results showed that acute dichlorvos administration did not cause marked cardiac damage, and oxidative stress probably does not play a major role in dichlorvos-induced poisoning. On the other hand, especially pralidoxime treatment markedly increased the serum total free sulfhydryl groups, paraoxonase and arylesterase activities. However, the underlying mechanisms for these changes are not exactly known. © 2010 Elsevier Inc.