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Lycopene, a Carotenoid, Attenuates Cyclosporine‐Induced Renal Dysfunction and Oxidative Stress in Rats
Author(s) -
Ateşşahin Ahmet,
Çeribaşı Ali Osman,
Yılmaz Seval
Publication year - 2007
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2007.00060.x
Subject(s) - lycopene , oxidative stress , thiobarbituric acid , nephrotoxicity , creatinine , glutathione , antioxidant , endocrinology , medicine , glutathione peroxidase , pharmacology , kidney , catalase , chemistry , biochemistry , lipid peroxidation , enzyme
The aim of this study was to investigate the possible protective role of antioxidant treatment with lycopene on cyclosporine A‐induced nephrotoxicity using biochemical and histopatological approaches. Adult male Sprague‐Dawley rats were randomly divided into four groups. The control group received physiological saline; animals in the lycopene group received only lycopene (10 mg/kg); animals in the cyclosporine A group received only cyclosporine A (15 mg/kg) and animals in cyclosporine plus lycopene group received cyclosporine and lycopene for 21 days. The effects of lycopene on cyclosporine A‐induced nephrotoxicity were evaluated by plasma creatinine, urea, sodium and calcium concentrations; kidney tissue thiobarbituric acid reactive species, reduced glutathione (GSH), glutathione peroxidase (GSH‐Px) and catalase activities and histopatological examinations. Administration of cyclosporine A to rats induced a marked renal failure, characterized with a significant increase in plasma creatinine and urea concentrations. Cyclosporine A also induced oxidative stress as indicated by increased kidney tissue concentrations of thiobarbituric acid reactive species and GSH, and reduced activities of GSH‐Px and catalase. Moreover, the kidneys of cyclosporine A‐treated rats showed tubular necrosis, degeneration, dilatation, thickened basement membranes, luminal cast formation and inter‐tubular fibrosis. Lycopene markedly reduced elevated plasma creatinine, urea levels and counteracted the deleterious effects of cyclosporine A on oxidative stress markers. In addition, lycopene ameliorated cyclosporine A‐induced pathological changes including tubular necrosis, degeneration, thickened basement membranes and inter‐tubular fibrosis when compared to the alone cyclosporine A group. These data indicate that the natural antioxidant lycopene might have protective effect against cyclosporine‐induced nephrotoxicity and oxidative stress in rat.