Cisplatin-induced nephrotoxicity is associated with oxidative stress, redox state unbalance, impairment of energetic metabolism and apoptosis in rat kidney mitochondria

N. A. G. Santos1, C. S. Catão1, N. M. Martins1, C. Curti2, M. L. P. Bianchi1, A. C. Santos1
1Departamento de Análises Clínicas, Toxicológicas E Bromatológicas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto – USP, Ribeirão Preto, Brazil
2Departamento de Física e Química, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, USP, Ribeirão Preto, Brazil

Tóm tắt

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 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 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.

Từ khóa


Tài liệu tham khảo

Antunes Greggi LM, Darin JD, Bianchi MD (2000) Protective effects of vitamin C against cisplatin-induced nephrotoxicity and lipid peroxidation in adult rats: a dose-dependent study. Pharmacol Res 41:405–411 Baek SM, Kwon CH, Kim JH, Jung JS, Kim YK (2003) Differencial roles of hydrogen peroxide and hydroxyl radical in cisplatin-induced cell death in renal proximal tubular epithelial cells. J Lab Clin Med 142:178–186 Baliga R, Zhang Z, Baliga M, Ueda N, Shah SV (1998) In vitro and in vivo evidence suggesting a role for iron in cisplatin-induced nephrotoxicity. Kidney Int 53:394–401 Berry MN, Edwards AM, Barritt GJ (1991) High-yield preparation of isolated hepatocytes from rat liver. In: Burdon RH, Knippenberg PH (eds) Laboratory techniques in biochemistry and molecular biology. Isolated hepatocytes preparation, properties and applications. Elsevier, Amsterdam, pp 15–58 Bowser DN, Petrou S, Panchal RG, Smart ML, Williams DA (2002) Release of mitochondrial Ca+2 via the permeability transition activates endoplasmic reticulum Ca+2 uptake. FASEB J 16:1105–1107 Brady HR, Kone BC, Stromski ME, Zeidel ML, Giebisch G, Gullans SR (1990) Mitochondrial injury: an early event in cisplatin toxicity to renal proximal tubules. Am J Physiol (Renal Fluid Electrolyte Physiol) 258:F1181–F1187 Cardoso SM, Pereira C, Oliveira R (1999) Mitochondrial function is differentially affected upon oxidative stress. Free Radic Biol Med 26:3–13 Chance B, Willians GR (1956) The respiratory chain and oxidative phosphorylation. Adv Enzymol 17:65–134 Chang B, Nishikawa M, Sato E, Utsumi K, Inoue M (2002) L-Carnitine inhibits cisplatin-induced injury of the kidney and small intestine. Arch Biochem Biophys 405:55–64 Conklin KA (2004) Cancer chemotherapy and antioxidants. J Nutr 134:3201S–3204S Cummings BS, Schnellmann RG (2002) Cisplatin-induced renal cell apoptosis: caspase 3-dependent and -independent pathways. J Pharmacol Exp Ther 302:8–17 Cvitkovic E (1998) Cumulative toxicities from cisplatin therapy and current cytoprotective measures. Cancer Treat Rev 24:265–281 Emaus RK, Grunwald R, Lemasters JJ (1986) Rhodamine-123 as a probe of transmembrane potential in isolated rat-liver mitochondria-spectral and metabolic properties. Biochim Biophys Acta 850:436–448 Fariss MW, Chan CB, Patel M, Van Houten B, Orrenius S (2005) Role of mitochondria in toxic oxidative stress. Mol Interv 5:94–111 Gallet PF, Maftah A, Petit JM, Denis-Gay M, Julien R (1995) Direct cardiolipin assay In yeast using the red fluorescence emission of 10-N-nonyl acridine orange. Eur J Biochem 15:113–119 Grattagliano I, Vendemiale G, Sabbá C, Buonamico P, Altomare E (1996) Oxidation of circulating proteins in alcoholics: role of acetaldehyde and xantine oxidase. J Hepatol 25:28–36 Hanigan MH, Devarajan P (2003) Cisplatin nephrotoxicity: molecular mechanisms. Cancer Ther 1:47–61 Hannemann J, Duwe J, Baumann K (1991) Iron and ascorbic acid-induced lipid peroxidation in renal microsomes isolated from rats treated with platinum compounds. Cancer Chemother Pharmacol 28:427–433 Hauff KD, Hatch GM (2006) Cardiolipin metabolism and Barth Syndrome. Prog Lipid Res 45:91–101 Hoffmann B, Stockl A, Schlame M, Beyer K, Klingenberg MJ (1994) The reconstituted ADP/ATP carrier activity has an absolute requirement for cardiolipin as shown in cysteine mutants. Biol Chem 269:1940–1944 Huang H, Zhu L, Reid BR, Drobny GP, Hopkins PB (1995) Solution structure of a cisplatin-induced DNA interstrand cross-link. Science 270:1842–1845 Kadikoylu G, Bolaman Z, Demir S, Balkaya M, Akalin N, Enli Y (2004) The effects of desferrioxamine on cisplatin-induced lipid peroxidation and the activities of antioxidant enzymes in rat kidneys. Hum Exp Toxicol 23:29–34 Kagan VE, Tyurina YY, Bayir H, Chu CT, Kapralov AA, Vlasova II, Belikova NA, Tyurin VA, Amoscato A, Epperly M, Greenberger J, Dekosky S, Shvedova AA, Jiang J (2006) The “pro-apoptotic genies” get out of mitochondria: oxidative lipidomics and redox activity of cytochrome c/cardiolipin complexes. Chem Biol Interact 163:15–28 Kaushal GP, Kaushal V, Hong X, Shah SV (2001) Role and regulation of caspases in cisplatin induced injury to renal tubular epithelial cells. Kidney Int 60:1726–1736 Li-Ping X, Skrezek C, Wand H, Reibe F (2000) Mitochondrial dysfunction at the early estage of cisplatin-induced acute renal failure in rats. J Zhejiang Univ Sci 1:91–96 Loeffler M, Kroemer G (2000) The mitochondrion in cell death control: certainties and incognita. Exp Cell Res 256:19–26 Lund BO, Miller DM, Woods JS (1993) Studies on Hg (II)- induced H2O2 formation and oxidative stress in vivo and in vitro in rat kidney mitochondria. Biochem Pharmacol 45:2017–2024 Masubuchi Y, Suda C, Horie T (2005) Involvement of mitochondrial permeability transition in acetaminophen-induced liver injury in mice. J Hepatol 42:110–116 Meyer AJ, Hell Rd (2005) Glutathione homeostasis and redox-regulation by sulfhydryl groups. Photosynth Res 86:435–457 Park SA, Park HJ, Lee BI, Ahn YH, Kim SU, Choi KS (2001) Bcl-2 blocks cisplatin-induced apoptosis by suppression of ERK-mediated p53 accumulation in B104 cells. Brain Res Mol Brain Res 93:18–26 Park MS, De Leon M, Devarajan P (2002) Cisplatin induces apoptosis in LLC-PK1 cells via activation of mitochondrial pathways. J Am Soc Nephrol 13:858–865 Pedersen PL, Grenawalt JW, Reynafarje B, Hullihen J, Decker GL, Soper JW, Bustamente E (1978) Preparation and characterization of mitochondria and submitochondrial particles of rat liver-derived tissues. Methods Cell Biol 20:411–481 Petit JM, Maftah A, Ratinaud MH, Julien R (1992) 10-N-nonyl acridine orange interacts with cardiolipin and allows the quantification of this phospholipid in isolated mitochondria. Eur J Biochem 209:267–273 Petrosillo G, Ruggiero FM, Paradies G (2003) Role of reactive oxygen species and cardiolipin in the release of cytochrome c from mitochondria. FASEB J 17:2202–2208 Sadzuka Y, Shoji T, Takino Y (1992) Mechanism of the increase in lipid peroxide induced by cisplatin in the kidneys of rats. Toxicol Lett 62:293–300 Santos AC, Uyemura SA, Santos NA, Mingatto FE, Curti C (1997) Hg(II)-induced renal cytotoxicity: in vitro and in vivo implications for the bioenergetic and oxidative status of mitochondria. Mol Cell Biochem 177:53–59 Scarpa A (1979) Measurements of cation transport with metallochromic indicators. In: Fleisher S, Packer L (eds) Methods in enzimology. Academic, New York, pp 301–352 Sedlak J, Lindsay RH (1968) Estimation of total, protein-bound, and nonprotein sulfhydryl groups in tissue with Ellman’s reagent. Anal Biochem 25:192–205 Shidoji Y, Hayashi K, Komura S, Ohishi N, Yagi K (1999) Loss of molecular interaction between cytochrome c and cardiolipin due to lipid peroxidation. Biochem Biophys Res Commun 264:343–347 Singh G (1989) A possible mechanism of cisplatin–induced nephrotoxicity. Toxicology 58:71–80 Somani SM, Husain K, Whitworth C, Trammell GL, Malafa M, Rybak LP (2000) Dose-dependent protection by lipoic acid against cisplatin-induced nephrotoxicity in rats: antioxidant defense system. Pharmacol Toxicol 86:234–241 Souid AK, Tacka KA, Galvan KA, Penefsky HS (2003) Immediate effects of anticancer drugs on mitochondrial oxygen consumption. Biochem Pharmacol 66:977–987 Sueishi K, Mishima K, Makino K, Itoh Y, Tsuruya K, Hirakata H, Oishi R (2002) Protection by a radical scavenger edaravone against cisplatin-induced nephrotoxicity in rats. Eur J Pharmacol 451:203–208 Tietze F (1969) Enzymic method for quantitative determination of nanogram amounts of total and oxidized glutathione: applications to mammalian blood and other tissues. Anal Biochem 27:502–522 Tuma R (2001) The two faces of oxygen. Sci Aging Knowledge Environ 2001:1–5 Ueda N, Kaushal GP, Shah SV (2000) Apoptotic mechanisms in acute renal failure. Am J Med 108:403–415 Wang D, Lippard SJ (2005) Cellular processing of platinum anticancer drugs. Nat Rev Drug Discov 4:307–320 Wang P, Song JH, Song DK, Ang J, Hao C (2006) Role of death receptor and mitochondrial pathways in conventional chemotherapy drug induction of apoptosis. Cell Signal 18:1528–1535 Zhang JG, Lindup WE (1994) Cisplatin nephrotoxicity: decreases in mitochondrial protein sulphydryl concentration and calcium uptake by mitochondria from rat renal cortical slices. Biochem Pharmacol 47:1127–1135 Zhang JG, Lindup WE (1996) Role of calcium in cisplatin-induced cell toxicity in rat renal cortical slices. Toxicology In Vitro 10:205–209 Zhang M, Mileykovskaya E, Dowhan W (2002) Gluing the respiratory chain together. Cardiolipin is required for supercomplex formation in the inner mitochondrial membrane. J Biol Chem 277:43553–43556 Zheng W, Sean R, Graziano JH (1998) Manganese inhibits mitochondrial aconitase: a mechanism of manganese neurotoxicity. Brain Res 799:334–342