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The pesticides are used in several fields of agriculture and farms to protect crops against harmful insects and herbs. The increased and uncontrolled use of these pollutants is very hazardous for the population health. Consumption of contaminated food matrices with these pesticides could impair the cell integrity and its molecular function. The main aim of this present study was to evaluate the alteration of the integrity of mitochondrial membranes and respiratory chain potential in the brain of rats exposed during 90 days to acetamiprid (AC), organochlorine of the new generation. After oral administration of AC in rats with 3.14 mg/kg of body weight, the results of this current study showed enhance in mitochondrial oxidative stress status by significant decrease of glutathione (GSH) level, glutathione pyroxidase (GPx), and catalase (CAT) activities. On the other hand, there is an increase in the enzymatic activity of the glutathione s-transferase (GST) and superoxide dismutase (SOD); at the same time, the MDA level was also highly increased. Furthermore, evaluation results of brain mitochondrial integrity revealed a significant increase in membrane permeability and mitochondrial swelling in rats exposed chronically to AC. Instead, other results of this present work showed a significant decrease in mitochondrial respiration potent (O consumption) in acetamiprid-treated rats. In conclusion, the long duration exposition of the animals to AC has led to respiratory chain dysfunction, disturbance of matrix oxidative status, and a loss of mitochondrial membranes integrity.

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The present work is to evaluate the neurotoxicity induced by pyrethroid insecticide "Deltamethrin" at 0.32 mg/kg/day in two main regions of the Wistar rat brain (hippocampus and striatum) and the protective effects of Quercetin at 10 mg/kg/day on this toxicity after 90 days of exposure. The assay of brain parameters showed that Deltamethrin caused a significant increase of mitochondrial metabolite level (proteins, lipids, and carbohydrates) and enzyme activity (glutathione S-transferase and superoxide dismutase); a decreased amount of mitochondrial glutathione level and catalase and glutathione peroxidase activities; and an increase of malondialdehyde (MDA) acid levels of the two regions. Furthermore, mitochondrial functional testing in the brains of treated rats exhibited a significant increase in permeability followed by a mitochondrial swelling. Instead, a statistically significant decrease in mitochondrial respiration (O consumption) was recorded in the striatum and hippocampus. Our study showed that the pesticide caused a significant increase of the cytochrome c amount correlated with activation of neuronal apoptosis mechanisms by the significant increase of caspase-3 of hippocampus and striatum. In particular, the results of behavioral tests (open field, classic maze tests of sucrose, and Morris water maze) have significant changes, namely bad behavior of the treated rats, affecting the level of anxiety, learning, and memory, and general motor activity has mainly been shown in treated rats. In addition, the histological cuts clearly confirm cerebral necrosis in the hippocampus and the striatum caused by the pesticide. They allow us to consider the necrotic areas, black spots, reduction, and denaturation of these brain regions in the treated rats. On the other hand, we have studied the protective effects against the neurotoxicity of Deltamethrin (DLM). In this context, after the gavage of Quercetin at the dose of 10 mg/kg/day, we have noticed an improvement in the entire parameters: mitochondrial enzyme, metabolic, histological, and behavioral parameters. This confirmed the improvement of preventive and curative effect of Quercetin against free radicals induced by the DLM.

No abstract