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Modulatory effects of glutathione on oxidative stress disorders induced by imidacloprid in rat brain
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Mohammad Sina Mirjani    , Mohammad Reza Khaksar * |
| Research Center for Environmental Pollutants, Qom University of Medical Sciences, Qom, Iran & Department of Occupational Health, Faculty of health, Qom University of Medical Sciences, Qom, Iran , mrkhaksar@muq.ac.ir |
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Abstract: (5 Views) |
Introduction: The widespread use of pesticides, especially neonicotinoid compounds such as imidacloprid, has increased agricultural production but poses serious environmental and neurological threats. Long-term exposure to imidacloprid causes the production of reactive oxygen species, increases lipid peroxidation, and impairs antioxidant and neuronal systems. Glutathione, as an endogenous antioxidant, plays an important protective role in reducing oxidative stress and maintaining neuronal function. The aim of this study was to investigate the effect of L-glutathione intervention in reducing oxidative and neurological disorders caused by short-term exposure to imidacloprid in rats.
Methods: 24 adults male Wistar rats were divided into four groups of 6: Sham group receiving saline, imidacloprid group at a dose of one-tenth of the LD50 (45 mg/kg), glutathione group at a dose of 100 mg/kg, and the combined imidacloprid + glutathione group. All treatments were performed daily for 28 days via gavage. After the end of the period, brain tissue was extracted and oxidative stress indices including lipid peroxidation (MDA), reduced glutathione (GSH) level, total antioxidant capacity (TAC), antioxidant enzyme activities (GPx, GSR, GST, SOD, CAT), and acetylcholinesterase (AChE) activity were measured.
Results: Imidacloprid administration significantly reduced the activities of AChE, TAC, GSH, and GPx, GSR, and GST enzymes, and increased MDA levels and SOD activity (p<0.05). Catalase activity was not affected. L-glutathione intake alone caused a relative increase in TAC and the activities of some antioxidant enzymes. In the combination group, L-glutathione intervention returned most oxidative and neurological indices to levels close to the control group, and a decrease in lipid peroxidation and an increase in antioxidant defense capacity were observed (p<0.01).
Conclusion: The results indicate that short-term exposure to imidacloprid causes oxidative stress and dysfunction in the nervous system. L-glutathione intervention effectively prevents oxidative damage and inhibits the activity of antioxidant enzymes, and modulates AChE activity. These findings confirm the protective role of glutathione in maintaining redox balance and reducing imidacloprid-induced neurotoxicity.
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| Keywords: Imidacloprid, glutathione, oxidative stress, rat brain |
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Type of Study: Research |
Subject:
General
Received: 2026/02/16 | Revised: 2026/05/17 | Accepted: 2026/05/17
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