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Alterations in Ca2+ homeostasis in rat erythrocytes with atrazine treatment: positive modulation by vitamin E

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Abstract

A very low level of intra-erythrocytic calcium content is very important for normal physiology of cells. In the present study, our main objective was to investigate the effects of atrazine toxicity on Ca2+ homeostasis and modulation by vitamin E. Experimental animals were orally administered atrazine (300 mg kg−1 body weight, daily) and vitamin E (100 mg kg−1 body weight, daily). All studies were carried out for 7, 14, and 21 days in male Wistar rats. Erythrocyte membranes were prepared and were analyzed for lipid peroxidation (LPO) and membrane bound ATPases. Furthermore, Ca2+ homeostasis was evaluated in erythrocytes. The present findings indicated that atrazine exposure induced oxidative stress which was associated with significant increase in lipid peroxidation (P < 0.05). Vitamin E treatment on the other hand significantly lowered the atrazine-induced lipid peroxidation. The increased LPO following atrazine exposure was accompanied by significant decrease in ATPases (P < 0.05) and disturbed Ca2+ homeostasis. Furthermore, vitamin E treatment had a beneficial effect by partially restoring ATPases and Ca2+ homeostasis. The current findings suggest that atrazine exerts its toxic effect by increasing LPO, altering the activity of membrane bound enzymes and disturbing Ca2+ homeostasis. Vitamin E treatment ameliorated the toxic effects of atrazine suggesting its role as a potential antioxidant.

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  1. Mohan Singh

    Present address: Department of Chemistry and Biology, University of Quebec at Trois-Rivieres, Trois-Rivieres, QC, G9A5H7, Canada

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  1. Department of Biochemistry, Basic Medical Science Block, Panjab University, Chandigarh, 160014, India

    Mohan Singh, Rajat Sandhir & Ravi Kiran

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Correspondence to Mohan Singh.

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Singh, M., Sandhir, R. & Kiran, R. Alterations in Ca2+ homeostasis in rat erythrocytes with atrazine treatment: positive modulation by vitamin E. Mol Cell Biochem 340, 231–238 (2010). https://doi.org/10.1007/s11010-010-0422-9

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  • DOI: https://doi.org/10.1007/s11010-010-0422-9

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