ArticleMolecular neurobiology2013
Zinc, a neuroprotective agent against aluminum-induced oxidative DNA injury.
Article in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 23 citations in OpenAlex.
- Computational drug design for neurosyphilis disease by targeting Phosphoglycerate Kinase in Treponema pallidum with enhanced binding affinity and reduced toxicity.Scientific reports · 2025Article
- Article
- Molecular mechanisms of aluminum neurotoxicity: Update on adverse effects and therapeutic strategies.Advances in neurotoxicology · 2021Article
- Synthesis of Quercetin-Metal Complexes, In Vitro and In Silico Anticholinesterase and Antioxidant Evaluation, and In Vivo Toxicological and Anxiolitic Activities.Neurotoxicity research · 2020Article
- Aluminum-induced "mixed" cell death in mice cerebral tissue and potential intervention.Neurotoxicity research · 2020Article
- Zinc Improves Cognitive and Neuronal Dysfunction During Aluminium-Induced Neurodegeneration.Molecular neurobiology · 2017Article
- Influence of zinc on calcium-dependent signal transduction pathways during aluminium-induced neurodegeneration.Molecular neurobiology · 2014Article
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2 authors at 1 institution in 1 country.
Funding
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Abstract
Aluminum (Al) has been considered as one of the most abundant elements and comprises nearly 8 % of the Earth's crust. Despite of its immense presence, studies regarding the molecular basis of its interaction with the physiological system are rather sparse. On the other hand, zinc (Zn), an essential micronutrient, has been regarded as the second most important metal for brain functioning. The objective of the present study was to investigate the protective potential of Zn, if any, during Al-induced detrimental effects on DNA, tritiated thymidine uptake as well as expression of stress marker genes and proteins in rat brain. Male Sprague-Dawley rats weighing 140-160 g were divided into four different groups viz.: normal control, Al treated (100 mg/kg b wt/day via oral gavage), Zn treated (227 mg/l in drinking water), and combined Al and Zn treated. All the treatments were carried out for a total duration of 8 weeks. Agarose gel electrophoresis revealed DNA laddering pattern and comets in the rat brain following Al treatment, which however, were attenuated upon Zn treatment. Further, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive cells, number of apoptotic brain cells, and uptake of tritiated thymidine were increased after Al treatment but were decreased upon Zn supplementation. Western blot and mRNA expressions of p53 and nuclear factor κB (NF-κB) were also found to be significantly elevated after Al treatment, which however, were reversed following Zn treatment. Hence, Zn shall prove to be an effective agent in mitigating the detrimental effects caused by Al in the rat brain.
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