Journal Title
Title of Journal: Arch Toxicol
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Abbravation: Archives of Toxicology
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Publisher
Springer-Verlag
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Authors: N A G Santos C S Catão N M Martins C Curti M L P Bianchi A C Santos
Publish Date: 2007/01/11
Volume: 81, Issue: 7, Pages: 495-504
Abstract
The clinical use of cisplatin cisdiamminedichloroplatinum II is highly limited by its nephrotoxicity The precise mechanisms involved in cisplatininduced mitochondrial dysfunction in kidney have not been completely clarified Therefore we investigated in vivo the effects of cisplatin on mitochondrial bioenergetics redox state and oxidative stress as well as the occurrence of cell death by apoptosis in cisplatintreated rat kidney Adult male Wistar rats weighing 200–220 g were divided into two groups The control group n = 8 was treated only with an intraperitoneal ip injection of saline solution 1 ml per 100 g body weight and the cisplatin group n = 8 was given a single injection of cisplatin 10 mg/kg body weight ip Animals were sacrificed 72 h after the treatment The cisplatin group presented acute renal failure characterized by increased plasmatic creatinine and urea levels Mitochondrial dysfunction was evidenced by the decline in membrane electrochemical potential and the substantial decrease in mitochondrial calcium uptake The mitochondrial antioxidant defense system was depleted as shown by decreased GSH and NADPH levels GSH/GSSG ratio and increased GSSG level Moreover cisplatin induced oxidative damage to mitochondrial lipids including cardiolipin and oxidation of mitocondrial proteins as demonstrated by the significant decrease of sulfhydryl protein concentrations and increased levels of carbonylated proteins Additionally aconitase activity which is essential for mitochondrial function was also found to be lower in the cisplatin group Renal cell death via apoptosis was evidenced by the increased caspase3 activity Results show the central role of mitochondria and the intensification of apoptosis in cisplatininduced acute renal failure highlighting a number of steps that might be targeted to minimize cisplatininduced nephrotoxicity
Keywords:
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