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 - applied biology tebessa university
2 - tebessa university

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.

References:

1. Kong B., Seog J.H., Graham L.M.,Lee S.P., 2011. Experimental considerations on the cytotoxicity of pesticide s. Nanomedicine. 6, 929–941.
2. Cronholm P., Karlsson HL., Hedberg J., Lowe TA., Winnberg L., Elihn K., Wallinder IO., Moller L., 2013. Intracellular uptake and toxicity of Ag and CuO pesticide s: a comparison between pesticide sands their corresponding metal ions. Small. 9, 970–982.
3. Vishwakarma V., Samal S.S., Manoharan N. 2010. Safety and risk associated with pesticide s-a review. Journal of Minerals and Materials Characterization and Engineering. 9(5), 455.
4. Dukhin A., Swasey S., Thommes M., 2013. A method for pore size and porosity analysis of porous materials using electroacoustics and high frequency conductivity. Colloids and Surfaces. 437, 127-132.
5. Clayton D.A., Doda J.N. and Freiberg E.C., 1974. The absence of a pyrimidine dimer repair mechanism in mammalian mitochondria. Proc. Natl Acad Sci USA. 71, 2777–2781.
6. Habig W.H., Pabst M.J., Jakoby W.B., 1974. Glutathione-S-transferase the first step in mercapturic acid formation. Journal of Biology and Chemistry. 249, 7130–9.
7. Aebi. 1984. Catalase. In L. Packer (Ed), methods in enzymology, Academic press, Orlando. 105, 121-126.
8. Flohé L., Günzler W.A. 1984. Assays of glutathione peroxidase. Methods Enzymol.105, 114-21.
9. Bradford M., 1976. A rapid and sensitive method for the quantities of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochemistry. 72, 24854.
10. Weckbercker G., Cory J.G., 1988. Ribonucleotide reductase activity and growth of Glutathione-depended mouse Leukemia L1210 cells in vitro. Cancer Letter. 40, 257-264. PMID: 3289734.
11. Warso M.A., Lands W.E., 1983. Lipid peroxidation in relation to prostacy clin and thromboxane physiology and pathophysiology. Br Med Bull. 277-280.
12. Beauchamp C., Fridovich I., 1971. Superoxide dismutase: improved assays and an assay applicable to acrylamide gels. Biochem. 44, 276-287.
13. Kristal B.S., Park B.K., Yu B.P., 1996. 4-Hydroxynonénal est un puissant inducteur de la transition de perméabilité mitochondriale. Biol Chem. 6033–6038.
14. Rouabhi R., Gasmi S., Boussekine S., Kebieche M., 2015. Hepatic Oxidative Stress Induced by Zn and Opposite Effect of Se in Oryctolagus cuniculus. J Environ Anal Toxicol. 289.
15. Henine S., Rouabhi R., Gasmi S., Amrouche A., Abide A., Salmi A., 2016. Oxidative stress status, caspase-3, stromal enzymes and mitochondrial respiration and swelling of Paramecium caudatum in responding to the toxicity of Fe3O4 pesticide s, Environ Health Sci. 8, 161.
16. Suchail S., Guez D., Belzunees L.P., 2009. Discrepancy between acute and chronic toxicity induced by imidacloprid and its metabolites in Apis mellifera. Environ Toxicol Chem. 20, 2482-2486.
17. Kowalczyk E., Kopff A., Kedziora J., Blaszczyk J., Kopff M., Niedworok J., Fijalkowski P. 2004. Pol J Environ Stud. 13(1), 41–43.
18. ATSDR (Agency for Toxic substances and Disease Registry). 2007, Fed. Regist. 12178–12179. [PubMed] [Google Scholar].
19. Al-Attar A.M., 2011 Antioxidant effect of vitamin E treatment on some heavy metals-induced renal and testicular injuries in male mice. Saudi J Biol Sci .18, 63–72.
20. Silva M.H., Gammon D., 2009. An assessment of the developmental, reproductive and neurotoxicity of endo sulfan. Birth Defects Res Dev Reprod Toxicol. 86, 1–28.
21. Cory-Slechta D., Thiruchelvam M., Ek R., Bk B., Brooks A., 2005. Developmental pesticide exposures and the Parkinson’s disease phenotype. Birth Defects Res A Clin Mol Teratol. 73, 136–139.
22. Gasmi S., Rouabhi R., Kebieche M., Salmi A., Boussekine S., Toualbia N., Taib C., Henine S., Bouteraa Z., Djabri B. 2016. Neurotoxicity of acetamiprid in male albino rats and the opposite effect of quercetin. Biotechnol Ind J. 12(7), 113.
23. Zouaoui S., Rouabhi R., Bouzenzana S., Menaceur F., Gasmi S., Benaicha B., 2023. Assessment of two steroid hormones Progestin and estrogen on cellular model Paramecium: oxidative stress, Mitochondrial swelling and kinetic. Researchsquare. https://doi.org/10.21203/rs.3.rs-3742249/v1
24. Ali C., Réda D.M., Rachid R., Houria B., 2009. Cadmium induced changes in metabolic function of mitochondrial isolated from potato tissue (Solanum tuberosum L.). American Journal of Biochemistry and Biotechnology. 5(1), 35-39
25. Shi H., Hudson L.G., Liu K.J., 2004. Oxidative stress and apoptosis in metal ion induced carcinogenesis. Free Radic Biol Med. 37, 582–593.
26. Assefa Z., Van Laethem A., Garmyn M., Agostinis P., 2005. Ultraviolet radiation induced apoptosis in keratinocytes: on the role of cytosolic factors. Biochim Biophys Acta. 1755, 90–106
27. Ivanina A.V., Habinck E., and Sokolova I.M., 2008. Differential sensitivity to cadmium of key mitochondrial enzymes in the eastern oyster, Crassostrea virginica gmelin (Bivalvia: Ostreidae). Comparative Biochemistry and Physiology - C Toxicology and Pharmacology. 148, 72-79.
28. Garceau N., Pichaud N., Couture P., 2010. Inhibition of goldfish mitochondrial metabolism by in vitro exposure to Cd, Cu and Ni. Aquatic Toxicology. 98, 107-112.
29. Wang Y., Fang J., Leonard S.S. and Rao K.M.K., 2004. Cadmium inhibits the electron transfer chain and induces reactive oxygen species. Free Radical Biology and Medicine. 36, 1434-1443.
30. Morris G., Berk M., 2015. Many roads to mitochondria dysfunction in neuro immune and neuropsychiatric disorders. BMC Med. 13, 68–75.
31. Rachid R., Djebar-Berrebbah H., Djebar M.R., 2008. Growth, chitin and respiratory metabolism of Tetrahymena pyriformis exposed to the insecticide Novaluron. Am Euras J Agric Environ Sci. 3, 873-881