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The study regarding effect of paraoxon on oxidative stress index in kidney tissue of rats

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Author(s): Maryam Abbasnezhad1 | Mahvash Jafari2 | Alireza Asgari3 | Reza Hajihoseini4 | Mansoureh Hajigholamali4 | Maryam Salehi5 | Mohammad Salimian1

Journal: Journal of Mazandaran University of Medical Sciences
ISSN 1735-9260

Volume: 19;
Issue: 73;
Start page: 17;
Date: 2009;
Original page

Keywords: Paraoxon | oxidative stress index | rat | kidney tissue

ABSTRACT
(Received 14 July, 2009 ; Accepted 23 December, 2009)AbstractBackground and purpose: Paraoxon is the active form of parathion, which is an organophosphate pesticide (OP). The toxic effects of some OPs are not limited to inhibition of cholinesterase, they are capable to produce free radicals and induce disturbance in body antioxidant systems. The purpose of this study was to evaluate the effect of paraoxon on oxidative stress index in the kidney of rat.Materials and methods: Wistar male rats were randomly divided in four groups including: control (corn oil as paraoxon solvent) and three paraoxon groups receiving different doses (0.3, 0.7 and 1mg/kg) by intraperitoneal injection. 24 hours after injection, animal was given anesthesia and kidney tissue removed. After kidney tissue hemogenation, superoxide dismutase (SOD) and catalase (CAT), lactate dehydrogenase (LDH) and glutathione S- transferase (GST) activities, glutathione (GSH) and malondialdehyde (MDA) levels were determined by biochemical methods.Results: At doses higher than 0.3 mg/kg paraoxon, kidney SOD and CAT activities were significantly increased, comparing with the control, while GSH level was significantly decreased. There were no significant changes observed in GST, LDH activities and MDA levels.Conclusion: The results suggest that paraoxon induces the production of free radicals and oxidative stress. The enhanced activity of antioxidant enzymes in kidney of rats probably was a function of the increased detoxification capacity. Depletion of tissue GSH is a prime factor, which can impair the cell’s defense against the toxic actions of free radicals.J Mazand Univ Med Sci 2009; 19(73): 17-26 (Persian).
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