Impact of Imidacloprid on the Mitochondrial Function of Wistar Rats’ Nervous System

Subject Areas : Journal of Chemical Health Risks

Sarra Zouaoui ¹ , Rachid Rouabhi ²

1 - Laboratory of Toxicology and Ecosystems Pathologies, Applied Biology Department, Echahid Cheikh Larbi Tebessi University, Tebessa, 12000, Algeria
2 - Laboratory of Toxicology and Ecosystems Pathologies, Applied Biology Department, Echahid Cheikh Larbi Tebessi University, Tebessa, 12000, Algeria

Received: 2024-05-05 Accepted : 2024-08-26 Published : 2024-09-24

Keywords: Imidacloprid, Pesticide, Neurotoxicity, Mitochondria, Apoptosis, Swelling, Oxidative stress,

Abstract :

Pesticides are chemicals used to struggle against harmful pests; they could affect any compartment after getting into nature. Most pesticides are made up of only a selective molecule. When compared to bulk materials like powders, plates, and sheets, pesticides have a relatively large specter-to-volume ratio because of their extremely potent chemical makeup. Because of this characteristic, pesticides might have unexpected chemical and physical characteristics because they interact with the molecules in the environment and compartment. The present assessment aims to test the neurotoxicity induced by a pesticide of Imidacloprid at 1.252 mM kg-1 per day in the Wistar rat’s brain. After gavage to the rats for 3 months in laboratory conditions of the groups (light/dark; humidity), tests on nervous system enzymes figured that pesticide caused a significant enhancement of inter-mitochondrial metabolites amount (proteins, fats, and carbohydrates) and mitochondrial enzyme activity (GST and SOD); decreased amount of mitochondrial GSH; an enhancement of mit-CAT and mit-GPx activity; a rise in MDA level. Mitochondrial functions of the treated Rat’s brains showed a notable rise in mitochondrial swelling and permeability. Rather, there was a statistically significant drop in the amount of oxygen consumed by mitochondrial respiration. All results confirm that the pesticide caused a dose-dependent response.

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