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Garlic and allopurinol alleviate the apoptotic pathway in rats’ brain following exposure to fipronil insecticide

Fipronil can cause oxidative tissue damage and apoptosis. Our goal is to evaluate the antiapoptotic impact of garlic or allopurinol against fipronil neurotoxicity. Thirty-six mature male albino rats were separated into control, garlic aqueous extract (500 mg/kg), allopurinol (150 mg/L in their drink...

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Detalles Bibliográficos
Autores principales: Bakr, Amira Abo, Ali, Mohamed, Ibrahim, Khairy
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Environmental Health and Toxicology & Korea Society for Environmental Analysis 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10014746/
https://www.ncbi.nlm.nih.gov/pubmed/36916050
http://dx.doi.org/10.5620/eaht.2022037
Descripción
Sumario:Fipronil can cause oxidative tissue damage and apoptosis. Our goal is to evaluate the antiapoptotic impact of garlic or allopurinol against fipronil neurotoxicity. Thirty-six mature male albino rats were separated into control, garlic aqueous extract (500 mg/kg), allopurinol (150 mg/L in their drinking water), fipronil (13.277 mg/kg), garlic+fipronil, and allopurinol+fipronil. Our results revealed that fipronil induced a significant increase in brain malondialdehyde, protein carbonyl levels as well as enzymatic antioxidant activities (superoxide dismutase, catalase, glutathione peroxidase, and xanthine oxidase), but glutathione-S-transferase recorded a significant decrease as compared to the control. In addition, fipronil significantly up-regulated the brain pro-apoptotic (Bax) and caspase-3 mRNA gene expression and induced DNA fragmentation but caused down-regulation in anti-apoptotic (Bcl-2) mRNA genes expression. Interestingly, co-administration with garlic or allopurinol improved the lipid peroxidation, antioxidant disturbance, and apoptosis induced by fipronil in the brain tissues. In conclusion, garlic or allopurinol reduced fipronil-induced apoptosis and reduced oxidative tissue damage, most likely through enhancing the tissue antioxidant defense system.