ArticleToxicology international2014
Coenzyme q10 abrogated the 28 days aluminium chloride induced oxidative changes in rat cerebral cortex.
Article in Toxicology international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Toward a Molecular Framework of Systemic Multi-Organ Toxicity Induced by Chronic Aluminum Chloride Exposure.Molecules (Basel, Switzerland) · 2026Review
- Nutraceuticals: A strategy to mitigate neurotoxicity.Advances in neurotoxicology · 2026Article
- Ameliorative and protective effects of coenzyme Q10 against natural and chemical toxicity: a narrative review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Antiamnesic Potential of Malvidin on Aluminum Chloride Activated by the Free Radical Scavenging Property.ACS omega · 2022Article
- Perfluorooctanoic acid affects mouse brain and liver tissue through oxidative stress.Arhiv za higijenu rada i toksikologiju · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe present study was designed to elucidate the impact of oral administration of aluminium chloride for 28 days with respect to oxidative stress in the cerebral cortex of female rats. Further, to investigate the potentials of Coenzyme (Co) Q10 (4, 8, and 12 mg/kg, i.p.) in mitigating the detrimental changes. MATERIALS AND
methodsBiochemical estimations of cerebral lipid peroxidation (LPO), reduced glutathione (GSH), vitamin E and activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were carried out after 28 days of aluminium chloride (AlCl3) and Co Q10 exposures along with histopathological examination of cerebral cortex of the rats.
resultsSubacute exposure to AlCl3(5 mg/kg) led to significant decrease in levels of GSH, vitamin E and activities of SOD, CAT, GPx, and an increase in LPO of cerebral cortex. These aberrations were restored by Co Q10 (12 mg/kg, i.p.). This protection offered was comparable to that of L-deprenyl (1 mg/kg, i.p.) which served as a reference standard. Histopathological evaluations confirmed that the normal cerebral morphology was maintained by Co Q10.
conclusionThus, AlCl3 exposure hampers the activities of various antioxidant enzymes and induces oxidative stress in cerebral cortex of female Wistar rats. Supplementation with intraperitoneal Co Q10 abrogated these deleterious effects of AlCl3.
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