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      Vitamin E, Vitamin C, or Losartan Is Not Nephroprotectant against Cisplatin-Induced Nephrotoxicity in Presence of Estrogen in Ovariectomized Rat Model

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          Abstract

          Background. The nephroprotective effect of vitamins E and C or losartan against cisplatin (CP)- induced nephrotoxicity when they are accompanied by estrogen was investigated. Methods. The ovariectomized rats received estradiol valerate for two weeks. At the end of the first week, a single dose of CP (7 mg/kg, IP) was also administered, and they received placebo (group 1), vitamin E (group 2), vitamin C (group 3), or losartan (group 4) every day during the second week, and they were compared with another three control groups. Results. CP alone increased the serum levels of blood urea nitrogen (BUN), creatinine (Cr), and kidney tissue damage score (KTDS), significantly ( P < 0.05), however at the presence of estradiol and CP, vitamin C, vitamin E, or losartan not only did not decrease these parameters, but also increased them significantly ( P < 0.05). The serum level of superoxidase dismutase (SOD) was reduced by CP ( P < 0.05), but it was increased when estradiol or estradiol plus vitamin C or losartan were added ( P < 0.05). Conclusion. The particular pharmacological dose of estrogen used in this study abolish the nephroprotective effects vitamins C and E or losartan against CP-induced nephrotoxicity.

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          TNF-α mediates chemokine and cytokine expression and renal injury in cisplatin nephrotoxicity

          Ganesan Ramesh, W. Brian Reeves (2002)
          Article 0 comments Cited 131 times – based on 0 reviews     Review now
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            TNF-alpha mediates chemokine and cytokine expression and renal injury in cisplatin nephrotoxicity.

            Ganesan Ramesh, W. Brian Reeves (2002)
            The purpose of these studies was to examine the role of cytokines in the pathogenesis of cisplatin nephrotoxicity. Injection of mice with cisplatin (20 mg/kg) led to severe renal failure. The expression of cytokines, chemokines, and ICAM-1 in kidney was measured by ribonuclease protection assays and RT-PCR. We found significant upregulation of TNF-alpha, TGF-beta, RANTES, MIP-2, MCP-1, TCA3, IL-1beta, and ICAM-1 in kidneys from cisplatin-treated animals. In addition, serum, kidney, and urine levels of TNF-alpha measured by ELISA were increased by cisplatin. Inhibitors of TNF-alpha production (GM6001, pentoxifylline) and TNF-alpha Ab's reduced serum and kidney TNF-alpha protein levels and also blunted the cisplatin-induced increases in TNF-alpha, TGF-beta, RANTES, MIP-2, MCP-1, and IL-1beta, but not ICAM-1, mRNA. In addition, the TNF-alpha inhibitors also ameliorated cisplatin-induced renal dysfunction and reduced cisplatin-induced structural damage. Likewise, TNF-alpha-deficient mice were resistant to cisplatin nephrotoxicity. These results indicate cisplatin nephrotoxicity is characterized by activation of proinflammatory cytokines and chemokines. TNF-alpha appears to play a central role in the activation of this cytokine response and also in the pathogenesis of cisplatin renal injury.
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              Cisplatin-induced nephrotoxicity is associated with oxidative stress, redox state unbalance, impairment of energetic metabolism and apoptosis in rat kidney mitochondria.

              N A G Santos, C Catão, N Martins … (2007)
              The clinical use of cisplatin (cis-diamminedichloroplatinum II) is highly limited by its nephrotoxicity. The precise mechanisms involved in cisplatin-induced 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 cisplatin-treated 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 (i.p.) 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, i.p.). 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 mitochondrial 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 caspase-3 activity. Results show the central role of mitochondria and the intensification of apoptosis in cisplatin-induced acute renal failure, highlighting a number of steps that might be targeted to minimize cisplatin-induced nephrotoxicity.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Nephrol
                Journal ID (iso-abbrev): Int J Nephrol
                Journal ID (publisher-id): IJN
                Title: International Journal of Nephrology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-214X
                ISSN (Electronic): 2090-2158
                Publication date (Print): 2012
                Publication date (Electronic): 26 September 2012
                Volume: 2012
                Electronic Location Identifier: 284896
                Affiliations
                1Water and Electrolytes Research Center, Isfahan University of Medical Sciences, HezarJerib Avenue, Isfahan 81745, Iran
                2Department of Physiology, Isfahan University of Medical Sciences, HezarJerib Avenue, Isfahan 81745, Iran
                3Kidney Diseases Research Center, Isfahan University of Medical Sciences, HezarJerib Avenue, Isfahan 81745, Iran
                4Department of Internal Medicine, Isfahan University of Medical Sciences, HezarJerib Avenue, Isfahan 81745, Iran
                5Department of Clinical Pathology, Isfahan University of Medical Sciences, HezarJerib Avenue, Isfahan 81745, Iran
                Author notes

                Academic Editor: James E. Springate

                Article
                DOI: 10.1155/2012/284896
                PMC ID: 3463913
                PubMed ID: 23056943
                SO-VID: a6c44522-a455-4ec6-bd06-9c5304b28da4
                Copyright © Copyright © 2012 Mehdi Nematbakhsh et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 12 June 2012
                Date revision received : 14 August 2012
                Date accepted : 20 August 2012
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Nephrology
                Data availability:
                ScienceOpen disciplines: Nephrology

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