Abstract

Background and Objective: Paraoxon (active metabolite of parathion) is one of the most toxic organophosphate (OP) compounds. Acetyl cholinesterase inhibition is the main acute toxic mechanisms of OPs. Free radicals production and disruption of antioxidant defense systems is one of non-cholinergic effects of these compounds. In the present study, the effect of acute paraoxon administration on the oxidative stress indices in rat liver and lactate dehydrogenase (LDH) activity in plasma and liver were evaluated. Methods: In the present study, 32 male Wistar rats (200-250 g) were randomly divided into 4 groups (6 animals in each group): control (corn oil as paraoxon solvent) and three experimental groups received different doses of paraoxon (0.07, 0.35, or 0.7 mg/kg body weight) intraperitoneally. Four hours after injection, under ether anesthesia, blood sample is given, liver tissue removed and transferred to liquid nitrogen. Superoxide dismutase (SOD), catalase (CAT), and LDH activities and the levels of glutathione (GSH) and malondialdehyde (MDA) were determined in liver tissue homogenates. Findings: Significant increase in SOD activity and decrease in CAT activity at doses of 0.35 and 0.7 mg/kg of paraoxon were observed (p<0.05). The level of glutathione significantly decreased in all doses of paraoxon. Paraoxon in all treatments induced significant increase in plasma LDH activity and decrease in liver LDH activity. MDA concentration did not show any significant alteration. Conclusion: Present Findings indicate that acute OP administration induces free radical generation, impairment of cell antioxidant balance and predispose the cells to oxidative stress. So measurement of plasma LDH activity might be a beneficial marker in OP toxicity.