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Article Publish Status: FREE
Abstract Title:

Tissues toxicity attenuation by vitamin E on oxidative damage induced by diazinon.

Abstract Source:

Environ Anal Health Toxicol. 2022 Dec ;37(4):e2022036-0. Epub 2022 Nov 10. PMID: 36916049

Abstract Author(s):

Kavoos Tahmasebi, Mahvash Jafari, Javad Heydari, Alireza Asgari, Maryam Salehi, Saeed Khazaie, Mohammad Saleh Abedini

Article Affiliation:

Kavoos Tahmasebi

Abstract:

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.

Study Type : Animal Study

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