Lycopene, a carotenoid, attenuates cyclosporine-induced renal dysfunction and oxidative stress in rats.
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.
Ateşşahin
Ahmet
A
Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Firat University, Elaziğ, Turkey. aatessahin@hotmail.com
Ceribaşi
Ali Osman
AO
Yilmaz
Seval
S
D058186:Acute Kidney Injury / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002118:Calcium / Q000097:blood; D002338:Carotenoids / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D016572:Cyclosporine / Q000009:adverse effects*; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D007166:Immunosuppressive Agents / Q000009:adverse effects*; D000077276:Lycopene; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014508:Urea / Q000097:blood
D000975:Antioxidants; D007166:Immunosuppressive Agents; D017392:Thiobarbituric Acid Reactive Substances; D002338:Carotenoids; D016572:Cyclosporine; D014508:Urea; D012964:Sodium; D003404:Creatinine; D002374:Catalase; D005979:Glutathione Peroxidase; D005978:Glutathione; D000077276:Lycopene; D002118:Calcium