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ORIGINAL ARTICLE
Year : 2016  |  Volume : 5  |  Issue : 3  |  Page : 176-182

Influence of ethanol on aluminum-induced alterations in oxidative stress of rat thalamic area


1 Department of Physiology, NRI Medical College and General Hospital, Chinakakani, Mangalagiri Mandal, Guntur District, Andhra Pradesh, India
2 Department of Physiology, Chettinad Hospital and Research Institute, Kelambakkam, Tamil Nadu, India
3 Department of Biochemistry, NRI Medical College and General Hospital, Chinakakani, Mangalagiri Mandal, Guntur District, Andhra Pradesh, India

Correspondence Address:
Prasunpriya Nayak
Department of Physiology, NRI Medical College and General Hospital, Chinakakani, Mangalagiri Mandal, Guntur District, Andhra Pradesh - 522 503
India
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Source of Support: ICMR Ad-hoc Research Grant to P Nayak, Institutional Support., Conflict of Interest: None


DOI: 10.4103/2277-8632.191837

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Background: Neurotoxic impacts of aluminum are associated with oxidant imbalance and implicated in many senile neurodegenerative disorders. Thalamus is relatively protected from aging-related issues, however, seldom studied. Aims: The study is aimed to find out the aluminum-induced oxidative stress in thalamic area and the influence of ethanol on that. Settings and Design: Influence of aluminum on oxidative stress parameters in the thalamic area has been studied in the presence of varied levels of ethanol exposures. Materials and Methods: Male Wistar rats were exposed to aluminum (10 mg/kg bw) and ethanol (0.8-1.6 g/kg bw). Thalamic levels of reduced glutathione (GSH) and lipid peroxidation thiobarbituric acid reactive substances (TBARS) were studied, along with the activities of superoxide dismutase (SOD), catalase, glutathione peroxidise (GPx), and glutathione reductase (GR). Statistical Analysis Used: The data were statistically analyzed using Kruskal-Wallis test for variance and the significance of the difference between groups was studied using Mann-Whitney U test. Results: Lone aluminum exposure failed to produce any alterations in all the tested parameters, except the GPx activity of thalamic area. Nevertheless, concomitant ethanol exposure caused significant alterations in those thalamic parameters barring GSH level and SOD activity. Maximum response was observed with the highest dose of ethanol exposure. Conclusions: Though thalamic area is reported to be selectively susceptible to aluminum-induced oxidative stress, concomitant presence of pro-oxidant dominance might have augmented the aluminum-induced oxidative stress there. The observation may help to understand the mechanistic riddle of oxidative stress created by aluminum, a redox-inactive metal.


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