ABSTRACT
The toxic effects of some organophosphate pesticides [Ops] which are capable to produce free radicals and induce disturbance in body antioxidant systems. Paraoxon is an OP that is the active form parathion. To evaluate the effect of paraoxon on liver antioxidant system of rat. Wister rats were randomly divided into four groups including: control [paraoxon solvent], and three groups receiving different doses of paraoxon [0.3, 0.7 and 1 mg/kg] by intraperitoneal injection. Animal were anesthetized and liver tissue removed 24 hours after injection. After hemogenation of liver tissue Superoxide Dismutase [SOD] and Catalase [CAT], Lactate Dehydrogenese [LDH] and Glutathione S- Transferase [GST] activities, Glutathione [GSH] and malondialdehyde [MDA] levels were determined by biochemical methods. Paraoxon increased CAT, LDH and SOD activities and MDA level at doses higher than 0.3 mg/kg, while GSH level was decreased significantly, as compare with the control group. GST activity was increased significantly at 0.3 and 0.7 mg/kg concentration [P<0.05], but at 1 mg/kg concentration was decreased as compare with the control group. Probably Paraoxon induced the production of free radicals and oxidative stress in a dose- dependent manner. The enhanced activity of antioxidant enzymes of liver is due to increase the detoxification capacity. Decrease of tissue GSH content indicatives of oxidative tissue injury and the increase of MDA level indicatives per oxidation that occurs in membranes of liver
Subject(s)
Animals, Laboratory , Lipid Peroxidation , Paraoxon , Antioxidants , Rats, WistarABSTRACT
The toxic effects of some Organophosphates [Ops] are not limited to inhibition of cholinesterase, they are capable to produce free radicals and induce disturbance in body antioxidant systems. Paraoxon is an OP, which is the active form of parathion. The aim of this study was to investigate the effects of paraxaon on oxidant-antioxidant system in rat brain tissue. Wistar rats were randomly divided into four groups [n=7] as followed: control [corn oil as paraoxon solvent] and three of groups of paraxaon receiving different doses [0.3, 0.7 and 1 mg/kg] by intraperitoneal injection. 24 hours after injection, animal to ether anesthesia and brain tissue removed. After brain 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. At doses higher than 0.3 mg/kg paraoxon, the enhanced activities of kidney SOD, CAT and GST and LDH activity [>/= 0.3 mg/kg] were significantly increased, comparing with the control, while GSH level was significantly decreased. There were no significant changes observed in MDA level. The results suggest that paraoxon induces the production of free radicals and oxidative stress in a dose- dependent manner. The enhanced activity of antioxidant enzymes in brain of rats probably as 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
Subject(s)
Animals, Laboratory , Male , Antioxidants , Rats, Wistar , Brain/metabolism , Oxidative StressABSTRACT
Background: the toxic effects of some Organophosphates [OPs] are not limited to inhibition of cholinesterase, they are capable to produce free radicals and induce disturbance in body antioxidant systems. Paraoxon is an OP, which is the active form of parathion. The aim of this study was to investigate the effects of paraxaon on oxidant-antioxidant system in rat brain tissue
Materials and Methods: wistar rats were randomly divided in to four groups [n=7] as followed: control [corn oil as paraoxon solvent] and three of groups of paraxaon receiving different doeses [0.3, 0.7 and 1 mg/kg] by intraperitoneal injection. 24 hours after injection, animal to ether anesthesia and brain tissue removed. After brain 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, the enhanced activities of kidney SOD, CAT and GST and LDH activity [>/= 0.3 mg/kg] were significantly increased, comparing with the control, while GSH level was significantly decreased. There were no significant changes observed in MDA level
Conclusions: the results suggest that paraoxon induces the production of free radicals and oxidative stress in a dose- dependent manner. The enhanced activity of antioxidant enzymes in brain of rats probably as 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
ABSTRACT
In the present study, the effects of intracuneiformis nucleus microinjection of gamma-aminobutyric acid4 [GABAA] receptor agonist and antagonist on antinociception inducced by morphine were investigated with formalin test in rat. Intracuneiformis nucleus microinjection of morphine [l0 ngr/rat] and Bicuculline [50, 100 ng/rat] induced antinociception in the both first and second phases of formalin test. Muscimol [25, 50, 100 ngr/rat] produced antinociception only in the second phase of formalin test. Morphine in combination with muscimol but not with bicuculline elicited potentiation. The responses induced by muscimol were not affected by bicuculline. The opioid receptor antagonist [naloxone] did not reduce the response induced by muscimol in the both first and second phases of formalin test. It may be concluded that central GABAA receptor stimulation induced antinociception in formalin test. However, the antinociception induced by GABAA receptor agonist may be partly mediated through nucleus cuneiformis opioid receptor mechanisms. The apparent antinociceptive effects of muscimol may be due to its leakage to rostal portion of Cnf and reduction in motion activity, so have no relation to its real antinociceptive effects