顺铂肾毒性损伤机制的研究进展
Research Advancement on Cisplatin-Induced Nephrotoxicity
DOI: 10.12677/WJCR.2012.24004, PDF, HTML, XML,  被引量 下载: 3,977  浏览: 18,487  科研立项经费支持
作者: 孙章萍:大连医科大学,大连;曲振运, 李墨林*:大连医科大学病理生理学教研室,大连
关键词: 顺铂肾毒性损伤Cisplatin; Nephrotoxicity; Injury
摘要: 顺铂(Cisplatin, DDP)是临床常用的细胞周期非特异性化疗药物,主要用于肺癌、睾丸癌、卵巢癌、膀胱癌、头颈部肿瘤等实质性恶性肿瘤的一线治疗。临床研究发现,DDP抗肿瘤作用的疗效与其用药剂量呈正相关,然而DDP剂量依赖性的肾毒性作用极大限制了其临床应用。但是剂量依赖性肾毒性作用极大限制了DDP的临床应用。至今为止DDP肾毒性损伤的作用机制尚不清楚,同时临床上也无可靠的、特异性的治疗方法。本文就DDP肾毒性损伤的变化和可能发生机制及其治疗对策进行综述,为进一步研究奠定基础。
Abstract: Cisplatin (DDP) is a cell cycle non-specific antineoplastic drug, which is generally preferred used for treating solid malignant tumors, including those originated in the head, neck, lung, testis, ovary, breast etc. It has been found that the antitumor effects of DDP were correlated with its dose; however, DDP-induced dose-dependent renal toxicity greatly limits its clinical application. Up to now the exact mechanism of nephrotoxicity induced by DDP remains un- known, and there were also no reliable and specific methods for treating or preventing DDP-induced acute renal injury yet. The information gleaned from this review may provide the changes and possible mechanism of DDP-induced nephrotoxicity and its therapeutic strategy for further research.
文章引用:孙章萍, 曲振运, 李墨林. 顺铂肾毒性损伤机制的研究进展[J]. 世界肿瘤研究, 2012, 2(4): 21-26. http://dx.doi.org/10.12677/WJCR.2012.24004

参考文献

[1] B. Rosenberg, L. VanCamp, J. E. Trosko and V. H. Mansour. Plati- num compounds: A new class of potent antitumour agents. Na- ture, 1969, 222(5191): 385-386.
[2] 潘琼婧, 乔树民. 几种铂制剂对体外培养食管癌细胞株(Eca109)作用的初步观察[J]. 北京医学, 1981, 3(3): 164-166.
[3] 高广猷. 抗癌新药——顺铂简介[J]. 新药与临床1983, 2(1): 23- 27.
[4] 蔡桂凤, 熊荣超, 赵丽嫣, 乔树民. 顺铂治疗晚期原发性卵巢恶性肿瘤[J]. 肿瘤防治研究, 1984, 11(2): 78-80.
[5] R. F. Ozols, R. C. Young. High-dose cisplatin therapy in ovarian cancer. Seminars in Oncology, 1985, 12 (4): 21-30.
[6] J. Sastry, S. J. Kellie. Severe neurotoxicity, ototoxicity and nephro- toxicity following high-dose cisplatin and amifostine. Pediatric Hematology-Oncology, 2005, 22(5): 441-445.
[7] F. Ries, J. Klastersky. Nephrotoxicity induced by cancer chemo-therapy with special emphasis on cisplatin toxicity. American Journal of Kidney Diseases, 1986, 8(5): 368-379.
[8] N. A. dos Santos, M. A. Carvalho Rodrigues, N. M. Martins and A. C. dos Santos. Cisplatin-induced nephrotoxicity and targets of nephroprotection: An update. Archives of Toxicology, 2012, 86(8): 1233-1250.
[9] C. L. Litterst, A. F. LeRoy and A. M. Guarino. Disposition and distribution of platinum following parenteral administration of cis-dichlorodiammineplatinum(II) to animals. Cancer Treatment Reports, 1979, 63(9-10): 1485-1492.
[10] N. Thatcher, H. Sharma, R. Harrison, A. Smith, A. Zaki, C. A. McAuliffe, D. Crowther and B. W. Fox. Blood clearance of three radioactively labelled platinum complexes: Cis-dichlorodiam- mine platinum II, cis, trans-dichlorodihy-droxy-bis-(isopropy- lamine) platinum IV, and cis-dichloro-bis-cyclopropylamine pla- ti-num II, in patients with malignant disease. Cancer Chemo- therapy and Pharmacology, 1982, 9(1): 13-16.
[11] D. Wang, S. J. Lippard. Cellular processing of platinum anti- cancer drugs. Nature Reviews Drug Discovery, 2005, 4(4): 307- 320.
[12] M. H. Hanigan, B. C. Gallagher and D. M. Townsend, V. Gabarra. Gamma-glutamyl transpeptidase accelerates tumor growth and increases the resistance of tumors to cisplatin in vivo. Carcinogenesis, 1999, 20(4): 553-559.
[13] M. H. Hanigan, E. D. Lykissa, D. M. Townsend, C. N. Ou, R. Barrios and M. W. Lieberman. Gamma-glutamyl transpeptidase- deficient mice are resistant to the nephrotoxic effects of cisplatin. American Journal of Pathology, 2001, 159(5): 1889-1894.
[14] C. Jacobs, S. M. Kalman, M. Tretton and M. W. Weiner. Renal handling of cis-diamminedichloro platinum (II). Cancer Treat- ment Reports, 1980, 64(12): 1223-1226.
[15] N. Pabla, R. F. Murphy, K. Liu and Z. Dong. The copper trans- porter Ctr1 contributes to cisplatin uptake by renal tubular cells during cisplatin nephrotoxicity. American Journal of Physiology —Renal Physiology, 2009, 296(3): F505-F511.
[16] G. Ciarimboli, T. Ludwig, D. Lang, H. Pavenstädt, H. Koepsell, H. J. Piechota, J. Haier, U. Jaehde, J. Zisowsky and E. Schlatter. Cisplatin nephrotoxicity is critically mediated via the human or- ganic cation transporter 2. American Journal of Pathology, 2005, 167(6): 1477-1484.
[17] R. M. Franke, A. M. Kosloske, C. S. Lancaster, K. K. Filipski, C. Hu, O. Zolk, R. H. Mathijssen and A. Sparreboom. Influence of Oct1/Oct2-deficiency on cisplatin-induced changes in urinary N- acetyl-beta-D-glucosaminidase. Clinical Cancer Research, 2010, 16(16): 4198-4206.
[18] D. M. Townsend, M. Deng, L. Zhang, et al. Metabolism of cis- platin to a nephrotoxin in proximal tubule cells. Journal of the American Society of Nephrology, 2003, 14(1):1-10.
[19] J. C. Gonzales-Vitale, D. M. Hayes, E. Cvitkovic and S. S. Stern- berg. The renal pathology in clinical trials of cis-platinum (II) diamminedichloride. Cancer, 1977, 39(4): 1362-1371.
[20] T. W. Jomes, S. Chopra, J. S. Kaujman, et al. Cis-diamminedi- chloroplatinum(Ⅱ)-induced acute renal failure in the rat. Corre- lation of structural and functional alterations. Laboratory Investigation, 1985, 52(4): 363-374.
[21] 谢立平, C. Skrezek, H. Wand. 顺铂肾毒性早期发病机理的初步研究[J], 实用肿瘤杂志, 1996, 11(6): 268-270.
[22] 李传刚, 刘文, 唐瑜等. 大剂量顺铂所致大鼠急性肾损害过程中内源性血管活性物质的动态变化及其意义[J]. 大连医科大学学报, 2008, 30(5): 420-422.
[23] J. A. Winston, R. Safirstein. Reduced renal blood flow in early cisplatin-induced acute renal failure in the rat. American Journal of Physiology, 1985, 249(4): F490-F496.
[24] R. E. Bulger, D. C. Dobyan. Proliferative lesions found in rat kidneys after a single dose of cisplatin. Journal of the National Cancer Institute, 1984, 73(5): 1235-1242.
[25] J. Yamate, K. Sato, M. Ide, M. Nakanishi, M. Kuwamura, S. Sakuma and S. Nakatsuji. Participation of different macrophage populations and myofibroblastic cells in chronicallydeveloped renal interstitial fibrosis after cisplatin-induced renal injury in rats. Veterinary Pathology, 2002, 39(3): 322-333.
[26] K. Sugihara, M. Gemba. Modification of cisplatin toxicity by an- tioxidants. Japanese Journal of Pharmacology, 1986, 40(2): 353- 355.
[27] H. Matsushima, K. Yonemura, K. Ohishi, A. Hishida. The role of oxygen free radicals in cisplatin-induced acute renal failure in rats. Journal of Laboratory and Clinical Medicine, 1998, 131(6): 518-526.
[28] N. A. Santos, C. S. Bezerra, N. M. Martins, C. Curti, M. L. Bianchi and A. C. Santos. Hydroxyl radical scavenger ameliorates cis- platin-induced nephrotoxicity by preventing oxidative stress, redox state unbalance, impairment of energetic metabolism and apop- tosis in rat kidney mitochondria. Cancer Chemotherapy and Phar- macology, 2008, 61(1): 145-155.
[29] G. Ramesh, W. B. Reeves. TNF-alpha mediates chemokine and cytokine expression and renal injury in cisplatinnephrotoxicity. Journal of Clinical Investigation, 2002, 110(6): 835-842.
[30] S. Faubel, E. C. Lewis, L. Reznikov, D. Ljubanovic, T. S. Hoke, H. Somerset, D. J. Oh, L. Lu, C. L. Klein, C. A. Dinarello and C. L. Edelstein. Cisplatin-induced acute renal failure is associated with an increase in the cytokinesinterleukin (IL)-1beta, IL-18, IL-6, and neutrophil infiltration in the kidney. Journal of Pharmacology and Experimental Therapeutics, 2007, 322(1): 8-15.
[31] 李传刚, 高华琨, 孙章萍等. 中性粒细胞在实验性小鼠肾毒性损伤中的变化及其意义[J]. 大连医科大学学报, 2011, 33(2): 111- 115.
[32] 舒晓宏, 潘明臣, 代菲菲等. 内毒素在大剂量顺铂所致大鼠急性肾损伤过程中的变化及意义[J]. 中国微生态杂志 2009, 21(6): 519-521.
[33] E. Pirotzky, C. Guilmard, C. Sidoti, F. Ivanow, P. Principe and P. Braquet. Platelet- activating factor antagonist, BN-52021 protects against cis-diamminedichloro-platinum nephrotoxicity in the rat. Ren Fail. 1990, 12(3): 171-176.
[34] D. R. Luke, K. Vadiei and G. Lopez-Berestein. Role of vascular congestion in cisplatin-induced acute renal failure in the rat. Nephrology Dialysis Transplantation, 1992, 7(1): 1-7.
[35] E. S. M. El-Sayed, M. F. Abd-Ellah and S. M. Attia. Protective effect of captopril against cisplatin-induced nephrotoxicity in rats. Pakistan Journal of Pharmaceutical Sciences, 2008, 21(3): 255-261.
[36] S. Saleh, A. A. Ain-Shoka, E. El-Demerdash and M. M. Khalef. Protective effects of the angiotensin II receptor blocker losartan on cisplatin-induced kidney injury. Chemotherapy, 2009, 55(6): 399-406.
[37] W. Lieberthal, V. Triaca and J. Levine. Mechanisms of death induced by cisplatin in proximal tubular epithelial cells: Apop- tosis vs. necrosis. American Journal of Physiology, 1996, 270(4): F700-F708.
[38] J. A. Gordon, V. H. Gattone II. Mitochondrial alterations in cis- platin-induced acute renal failure. American Journal of Physiol- ogy, 1986, 250(6): F991-F998.
[39] M. Kruidering, B. Van de Water, E. de Heer, G. J. Mulder and J. F. Nagelkerke. Cisplatin-induced nephrotoxicity in porcine proxi- mal tubular cells: Mitochondrial dysfunction by inhibition of com- plexes I to IV of the respiratory chain. Journal of Pharmacology and Experimental Therapeutics, 1997, 280(2): 638-649.
[40] R. H. Lee, J. M. Song, M. Y. Park, S. K. Kang, Y. K. Kim and J. S. Jung. Cisplatin-induced apoptosis by translocation of endoge- nous Bax in mouse collecting duct cells. Biochemical Pharmacology, 2001, 62(8): 1013-1023.
[41] L. Cilenti, G. A. Kyriazis, M. M. Soundarapandian, V. Stratico, A. Yerkes, K. M. Park, A. M. Sheridan, E. S. Alnemri, J. V. Bon- ventre and A. S. Zervos. Omi/HtrA2 protease mediates cisplatin- induced cell death in renal cells. American Journal of Physiol- ogy—Renal Physiology, 2005, 288(2): F371-F379.
[42] R. Seth, C. Yang, V. Kaushal, S. V. Shah and G. P. Kaushal. p53- dependent caspase-2 activation in mitochondrial release of apo- ptosis-inducing factor and its role in renal tubular epithelial cell injury. Journal of Biological Chemistry, 2005, 280(35): 31230- 31239.
[43] G. Ramesh, W. B. Reeves. TNFR2-mediated apoptosis and necro- sis in cisplatin-induced acute renal failure. American Journal of Physiology—Renal Physiology, 2003, 285(4): F610-F618.
[44] S. Camano, A. Lazaro, E. Moreno-Gordaliza, A. M. Torres, C. de Lucas, B. Humanes, J. A. Lazaro. M. M. Gomez-Gomez, L. Bosca and A. Tejedor. Cilastatin attenuates cisplatin-induced proxi- mal tubular cell damage. Journal of Pharmacology and Experi- mental Therapeutics, 2010, 334(2): 419-429.
[45] N. Morishima, K. Nakanishi, H. Takenouchi, T. Shibata and Y. Yasuhiko. An endoplasmic reticulum stress-specific caspase cas- cade in apoptosis. Cytochrome c-independent activation of cas- pase-9 by caspase-12. Journal of Biological Chemistry, 2002, 277(37): 34287-34294.
[46] M. Peyrou, P. E. Hanna and A. E. Cribb. Cisplatin, gentamicin, and p-aminophenol induce markers of endoplasmic reticulum stress in the rat kidneys. Journal of Toxicological Sciences, 2007, 99(1): 346-353.
[47] P. Benoehr, P. Krueth, C. Bokemeyer, A. Grenz, H. Osswald and J. T. Hartmann. Nephroprotection by theophylline in patients with cisplatin chemotherapy: A randomized, single-blinded, placebo- controlled trial. Journal of the American Society of Nephrology, 2005, 16(2): 452-458.
[48] M. Naziroglu, A. Karaoğlu and A. O. Aksoy. Selenium and high dose vitamin E administration protects cisplatin-induced oxida- tive damage to renal, liver and lens tissues in rats. Toxicology, 2004, 195(2-3): 221-230.
[49] 冯乐平, 乔伟. 顺铂诱导肾小管上皮细胞程序性死亡的机理[J]. 吉林大学学报, 2008, 34(4): 581-584.
[50] M. Li, S. Balamuthusamy, A. M. Khan, et al. Pituitary adenylate cyclase-activating polypeptide prevents cisplatin-induced renal failure. Journal of Molecular Neuroscience, 2011, 43(1): 58-66.
[51] 李传刚, 张萌佳, 舒晓宏等. 吡咯烷二硫氨基甲酸对小鼠大剂量顺铂肾毒性损伤的防治作用[J]. 大连医科大学学报, 2010, 32(4): 388-391.