Diazinon (DZN) as an organophosphate pesticide may cause oxidative stress in different tissues. Antioxidants increase tissue protection from oxidative stress. The aim of the present study was to investigate prophylactic and therapeutic effects of vitamin C against oxidative stress caused by DZN in various tissues of male Wistar rats. Thirty rats were divided into five groups: control group received corn oil as DZN solvent, DZN group received 100 mg/kg of DZN, C group received 200 mg/kg of vitamin C, C‐DZN and DZN‐C groups received vitamin C before and after DZN injection. Plasma and various tissues were prepared and evaluated for measurement of the biochemical parameters and oxidative stress biomarkers. Results showed that acute administration of DZN significantly increased superoxide dismutase and glutathione‐S‐transferase activities and malondialdehyde level in all tissues, catalase (CAT) activity in liver, kidney and heart and some plasma biochemical indices, while it decreased cholinesterase and lactate dehydrogenase activities and glutathione content in all tissues. CAT activity in erythrocytes, brain and spleen was decreased in DZN‐exposed rats compared with the control group. Administration of vitamins C in both prophylactic and therapeutic groups ameliorated in these parameters, although all these tests in tissues did not return to the normal level. These data suggest that oxidative stress is an essential mechanism involved in DZN‐induced adversity effect, as evidenced by the altered activity of antioxidant enzymes, depleted GSH content and the enhanced membrane lipid peroxidation. Both the prophylactic and therapeutic treatments of rats to vitamin C have beneficial effects against oxidative stress and cholinergic hyperactivity induced by DZN in tissues especially in the brain tissue through free radical scavenging.
Background:
Exposure to diazinon (DZN) as an organophosphorus insecticide associates with reducing the
antioxidant capacity of cells. N-acetyl cysteine (NAC) is widely used in clinics to treat several diseases related to oxidative
stress.
Objective:
The current study was aimed to evaluate the prophylactic and therapeutic roles of NAC on biochemical and
oxidative changes induced by acute poisoning of DZN in various tissues of male Wistar rats.
Methods:
Thirty rats were divided into five groups: control group received corn oil as DZN solvent; DZN group received
100 mg/kg of DZN; NAC group received 160 mg/kg of NAC; NAC-DZN and DZN-NAC groups received 160 mg/kg of
NAC before and after 100 mg/kg of DZN injection, respectively. Plasma and various tissues were prepared and evaluated
for measurement of the biochemical parameters and oxidative stress biomarkers.
Results:
Both prophylactic and therapeutic treatments by NAC ameliorated the increased lipid peroxidation and decreased
glutathione level and superoxide dismutase, catalase and glutathione S-transferase activities in tissues (P<0.05). Moreover,
treatment with the NAC caused significant reduction in DZN-induced high levels of plasma biochemical parameters.
Furthermore, acetylcholinesterase activity was positively correlated with both LDH (P=0.000) activity and GSH (P=0.001)
level and negatively correlated with MDA (P=0.009) level in brain.
Conclusion:
Results suggest that NAC could effectively ameliorate the DZN-induced oxidative stress and cholinergic
hyperactivity in various tissues especially in the brain through free radicals scavenging and GSH synthesis. Prophylactic
approach exerted a stronger protective effect compared to therapeutic treatment.
Organophosphorus insecticides such as diazinon (DZN) are used worldwide in industry, veterinary practice, and agriculture. They may induce oxidative stress in different tissues. The use of antioxidants can protect tissues against oxidative stress. The aim of this study was to investigate the prophylactic and therapeutic roles of vitamin E against DZN–induced oxidative damage and biochemical alterations in various tissues of male Wistar rats. Thirty rats were divided into five groups: Control group received only corn oil as DZN solvent, DZN group received 100 mg/kg of DZN, E group received 150 mg/kg of vitamin E, E-DZN group received vitamin E and then dosed with DZN and DZN-E group received DZN and then dosed with vitamin E. All injections were carried out intraperitoneally. Plasma and various tissues were prepared and evaluated. Results showed that acute administration of DZN caused a significant induction of oxidative damage in the tested tissues via increased malondialdehyde level and some plasma biochemical indices, depletion of glutathione (GSH), reduced cholinesterase activity and change in the activities of superoxide dismutase, catalase and glutathione-S transferase. Treatment of rats with vitamin E resulted in an elevation in the level of GSH, normalizing the antioxidant enzymes activities and decreasing lipid peroxidation, although all these tests did not return to the normal level in certain tissues. The findings of this study suggest that both prophylactic and therapeutic treatments of rats with vitamin E provide a protective role against DZN-induced oxidative stress and cholinergic hyperactivity through free radicals scavenging and membrane stabilizing.
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