Thymol abates the detrimental impacts of imidacloprid on rat brains by lessening oxidative damage and apoptotic and inflammatory reactions.

Autor: Abd-Elhakim YM; Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Zagazig University, Zagazig, 44519, Egypt. Electronic address: yasmina_forensic@hotmail.com., Saber TM; Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Zagazig University, Zagazig, 44519, Egypt. Electronic address: taghredsaber1982@gmail.com., Metwally MMM; Department of Pathology, Faculty of Veterinary Medicine, Zagazig University, Zagazig, 44519, Egypt., Abd-Allah NA; Clinical Pathology Department, Faculty of Veterinary Medicine, Zagazig University, Zagazig, 44519, Egypt., Mohamed RMSM; Department of Clinical Pharmacology, Faculty of Medicine, Zagazig University, Zagazig, Egypt., Ahmed GA; Forensic Medicine & Clinical Toxicology Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
Jazyk: angličtina
Zdroj: Chemico-biological interactions [Chem Biol Interact] 2023 Sep 25; Vol. 383, pp. 110690. Date of Electronic Publication: 2023 Aug 28.
DOI: 10.1016/j.cbi.2023.110690
Abstrakt: Imidacloprid (IMID) is one of the most widely used neonicotinoid insecticides globally and, consequently, a probable widespread environmental contaminant. The potential neurotoxic effects of IMID have been previously reported. This study aimed to investigate the possible beneficial effect of thymol (TML) in relieving IMID-induced harmful effects on the brain of male Sprague-Dawley rats. For this aim, four groups (10 rats/group) were orally administered corn oil, TML (30 mg/kg b.wt), IMID (22.5 mg/kg b.wt), or TML + IMID for 56 days. The brain tissues were biochemically, histopathologically, and immunohistochemically evaluated. The results displayed that TML significantly restored the IMID-induced depletion of the total antioxidant capacity of the brain tissues. At the same time, the IMID-associated increased levels of lipid peroxidation in terms of malondialdehyde content were markedly suppressed in the TML + IMID group. Also, TML oral dosing markedly reduced the release of inflammatory elements, including nitric oxide and myeloperoxidase, resulting from IMID exposure. Furthermore, the IMID-induced decrease in gamma-aminobutyric acid but the increase in acetylcholinesterase was considerably reversed by TML oral dosing. Additionally, TML oral administration significantly counteracted the IMID-induced brainepatic DNA damage, as revealed by the comet assay. Besides, a significant downregulatibrainepatic Caspase-3 was evident in the TML + IMID group compared to the IMID group. However, TML oral dosing has not significantly altered the IMID-induced nuclear factor (NF-κB p65) increase. Therefore, TML could be a protective agent against IMID-induced detrimental impacts on brain tissue, possibly through its antioxidant, antiapoptotic, and anti-inflammatory activities.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2023 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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