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ARTICLE

Alpha-Tocopherol Supplementation Restricts Aluminium- and Ethanol-Induced Oxidative Damage in Rat Brain but Fails to Protect Against Neurobehavioral Damage

, MSc (Sci), PhD (Sci), MSc (Med), PhD (Med), , MBBS, PhD (Med) & , MBBS, MD
Pages 257-268 | Published online: 05 Apr 2018
 

ABSTRACT

The concurrent presence of oxidative stress (OS) and aluminium exposure is an inducer of neurodegenerative changes. Aluminium can augment OS in a pro-oxidant dominant condition. Antioxidative property of α-tocopherol may be useful in restricting these degenerative changes in the brain. OS parameters are tested in frontal cortex (FC), hippocampus (HC), and cerebellum (CL) of α-tocopherol-supplemented (5 IU/day) male Wistar rats exposed to aluminium (10 mg Al/Kg/day; “Al”), ethanol (0.6 g ethanol/Kg/day; “Et”), and both (“Al-Et”) and vehicle-treated control (“C”) for 4 weeks. The α-tocopherol supplementation restricted regional alterations of reduced glutathione, superoxide dismutase, catalase, and glutathione peroxidase. Accordingly, the regional superoxide and peroxide handling capacities (SPHC) also remain unaltered. Al-Et group demonstrated significant elevation in the lipid peroxidation level in FC and CL regions compared to the group C; similar elevations in lipid peroxidation were noted in all the tested brain regions of Al group. Likewise, declines in glutathione reductase activity were noted in HC (versus Et group) and CL (versus Al and Et groups) of Al-Et group. Interestingly, changes in behavioral patterns of all the treatment groups are comparable while differing from that of the control group. Significant difference with group C is observed during first through fourth weeks, third to fourth weeks, and second to third weeks in terms of spontaneous motor activity, Rota Rod performance, and Hebb-Williams maze performance, respectively. Hence, the current dose and duration of α-tocopherol supplementation failed to provide full protection against the aluminium-induced neurodegeneration; nevertheless, it could provide only partial protection toward aluminium-induced augmentation of OS in specific brain regions.

Declaration of interest

The authors declare no conflicts of interest. The authors alone are responsible for the content and writing of the article.

Additional information

Funding

Indian Council of Medical Research (IRIS ID No. 2010-20650)

Notes on contributors

Prasunpriya Nayak

Dr. Prasunpriya Nayak, MSc (Physiology), PhD (Physiology), MSc (Medical Physiology), PhD (Medical Physiology). Associate Professor, Department of Physiology, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India; Research Interest - Neurotoxicology, Neurodegenerative disorders, Wound healing, Oxidative stress.

Shiv Bhushan Sharma

Dr. Shiv Bhushan Sharma, MBBS, PhD (Medical Physiology), Professor, Department of Physiology, Chettinad Hospital and Research Institute, Kelabakkam, Chennai-603103, India. Research Interest - Neurophysiology, Yoga.

N V S Chowdary

Dr. N V S Chowdary, MBBS, MD. Professor, Department of Biochemistry, NRI Medical College, Guntur 522503, Andhra Pradesh, India. Research Interest - Brain Biochemistry, Clinical biochemistry.

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