الفهرس 
Introduction and Aim of workOnly 14 pages are availabe for public view
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Abstract
The hazards of accidental exposure to ionizing radiation become series mater nowadays and crisis like Chernobyl crisis at 1986 and Fukushimas Nuclear power plant disaster at 2011 left deep impact on the human health and environment. Also, exposure to pesticides and other agrochemicals constitutes one of the major occupational risks. The use of pesticides was found to be accompanied with various adverse effects to human health. Organophosphorus insecticides produce its toxic effect through inhibition of AChE in brain of insects and human however organophosphates may produce cytotoxicity and genotoxicity in mammals. In addition, there are accumulated evidences suggested that oxidative stress may involve in organophosphates toxicity
It is proposed that glutathione could control the capacity of hepatocytes in eliminating the adverse effect of such pollutants under acute exposure condition. The study was aimed to examine the correlation between the depletion of GSH and the activity of the esterases
enzymes and the role of increased GSH to reduce the cytotoxic effect of these potent agents. Experimental design, treatment groups and biochemical parameters: Chemicals Buthionine sulfoximine (BSO) a specific inhibitor of GSH bio-synthesis was used as single dose of 200 mg/kg body weight dissolved in saline solution one hour before Chlorpyrifos and/or gamma ray treatment. N-acetylcystein (NAC), a pre-courser of GSH and anti-oxidant agent was used (a single dose of 200 mg/kg boy weight) one hour before Chlorpyrifos and/or gamma ray treatment. Chlorpyrifos (CPF), an organophosphorus insecticide was used as a single dose of 30 mg/kg body weight dissolving in corn oil. Gamma ray exposure procedure Groups of animals exposed to a single whole body dose of 6 Gy of gamma ray.
Animal groups and treatment: Adult male albino rats (84 animals) were divided into 12 groups (7animals/group) and received treatment as follow: Group 1: Rats received single oral dose of corn oil (1 ml/kg) as a control group. Group 2: Rats received single oral dose of CPF dissolved in corn oil. Group 3: Rats were orally administrated with single dose of BSO in normal saline in addition to single oral dose of corn oil. Group 4: Rats were orally administrated with single dose of BSO one hour before receiving single oral dose of CPF. Group 5: Rats were orally administrated with single dose of NAC in addition to single oral dose of corn oil. Group 6: Rats were orally administrated with single dose of NAC one hour before receiving single oral dose of CPF. Group 7: Rats were exposed to a single whole body gamma irradiation (6 Gy).
Group 8: Rats were exposed to a single whole body gamma irradiation (6 Gy) just after receiving single oral dose of CPF. Group 9: Rats were exposed to a single whole body gamma irradiation (6Gy) one hour after receiving single oral dose of in addition to single oral dose of corn oil. Group 10: Rats were received single oral dose of BSO and after one hour rats were received CPF followed by exposure to a single whole body gamma irradiation (6Gy). Group 11: Rats were exposed to a single whole body gamma irradiation (6 Gy) one hour after receiving single oral dose of NAC in addition to single oral dose of corn oil. Group 12: Rats were received single oral dose of NAC and after one hour rats were received CPF followed by exposure to a single whole body gamma irradiation.
Summary
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Samples and biochemical parameters: After 24 hours from last treatment blood sample withdrawn and animal’s brain and liver removed and subjected to the biochemical examination, the following parameters were determined: 1- Reduced Glutathione (GSH) level. 2- Glutathione-S- transferase (GST) activity. 3- Glutathione Reductse (GR) activity. 4- Acetylchlonesterase (AChE) Activity. 5- Carboxyleaterase (CE) Activity. 6- Paraoxonase (PON) activity. 7- Arylesterase (AE) activity. 8- Native PAGE electrophoresis for Carboxylesterase isozymes in plasma, liver and brain. 9- Native PAGE electrophoresis for Paraoxonase isozymes in plasma, liver and brain. Results:
The result indicated that CPF produced no change in GSH level. Treatment with either BSO and CPF and IR produced decrease in GSH level in plasma. NAC restored GSH level near the control level in all treated groups, CPF had no effect on GST and pre-treatment with either BSO or NAC increased GST activity in CPF treated groups. Exposure to IR had no effect on GST. Rats treated with CPF or NAC or BSO followed by γ-rays exposure showed inhibition in plasma GST activity and activation the level of liver GST. Treatment with NAC followed by CPF had decreasing effect on GST activity in brain. While rats with the same treatment followed by γ-radiation exposure showed an increase in GST activity in brain tissue. Treatment with either BSO or NAC produced inhibition in plasma and liver GR activities in CPF treated groups. No change was observed in GR activities of plasma, liver and brain in all the IR-exposed groups. Treatment with CPF inhibited AChE activity in plasma, liver and brain. Whereas exposure to IR inhibited AChE in brain only. Pre-treatment with either BSO or NAC increased the inhibitory effect of CPF. On AChE activity in plasma, liver and brain. Whereas, exposure to
IR improved the activity of AChE in plasma, liver and brain. Treatment with CPF inhibited CE activity in plasma, liver and brain. Whereas, exposure to IR increased the activity in liver. Pretreatment with BSO had no effect on CPF-produced inhibition whereas, NAC reduced the inhibitory effect. Exposure to IR improved the activity of AChE in plasma and brain with least extent in liver. On the other hand CPF produced no change in plasma and brain PON activity whereas liver PON activity was inhibited. Treatment with BSO or NAC had no effect on the inhibition produced by CPF. In contrast, exposure to IR increased PON activity and improved the activity in CPF treated groups. Treatment with CPF increased plasma AE activity while AE activity was decease in liver and brain tissues. Either BSO or NAC could minimize this effect. In liver, CPF inhibited AE activity and pre-treatment with either BSO or NAC decreased this inhibitory effect. Exposure to IR increased AE activity and improved the activity in CPF treated groups. The native PAGE electrophoresis for CE and PON isozyme confirm the biochemical results.