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DOKSORUBİSİN KARDİYOTOKSİSİTESİNİN OLUŞUMU VE ÖNLENMESİ

Year 2021, Volume: 4 Issue: 1, 1 - 15, 30.05.2021

Zeynep Erdoğmuş Özgen

https://doi.org/10.52538/iduhes.827754
Cited By: 1

Abstract

Yüksek antineoplastik aktiviteleri nedeniyle onkolojide en sık kullanılan antrasiklinler arasında yer alan doksorubisin; göğüs, over, testis, tiroid, akciğer kanserlerinde ve birçok sarkomun tedavisinde klinik uygulaması olan önemli ilaçlardan biridir. Ancak doksorubisinin klinik kullanımını kısıtlayan önemli ve ciddi kardiotoksik yan etkisi vardır. Bu derlemede kardiotoksik etki mekanizmasının araştırılması amaçlandı. Araştırma sonucunda kardiotoksisite oluşumunda; nükleik asit ve protein sentezinin inhibisyonu, vazoaktif aminlerin salınımı, mitokondriyal membran potansiyelinde kayıp ve elektron trasport zincirinin inhibisyonu, adrenerjik fonksiyonlardaki değişiklikler, adenilat siklaz, Na+-K+ ATPaz ve Ca+ ATPaz aktivitelerinin azalması gibi mekanizmalar etkili olsa da oksidatif stres ve apoptozisin asıl etken olduğu görülmüştür. Doksorubisinin oluşturduğu kardiotoksisiteyi azaltmaya yönelik koruyucu maddeler araştırmalarda kullanılmış olsa da bu maddelerin klinikte kullanımları yeterli düzeylere ulaşılabilmiş değildir. Yapılan literatür taraması sonucunda, Doksorubisinin oluşturduğu kardiotoksisiteyi azaltmaya yönelik daha ayrıntılı çalışmaların yapılması gerektiği kanaatine varılmıştır.

Keywords

Doksorubisin Kardiotoksisite Oksidatif stress Apoptozis

Supporting Institution

YOK

Project Number

YOK

References

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  • Ma, J., Wang, Y., Zheng, D., Wei, M., Xu, H., Peng, T.(2013). Rac1 signalling mediates Doksorubisin-induced cardiotoxicity through both reactive oxygen species-dependent and-independent pathways. Cardiovasc Res, 1;97(1):77-87.
  • Minotti, G., Recalcati, S., Menna, P., et al.(2004). Doxorubicin cardiotoxicity and the control of iron metabolism: quinone-dependent and independent mechanisms. Methods Enzymol, 378: 340-361.
  • Moens, AL., Leyton-Mange, JS., Niu, X., Yang, R., Cingolani, O., Arkenbout, EK. et al.(2009). Adverse ventricular remodeling and exacerbated NOS uncoupling from pressure-overload in mice lacking the beta3-adrenoreceptor. J Mol Cell Cardiol, 47: 576–585.
  • Morishima, I., Okumura, K., Matsui, H. et al. (1999). Zinc accumulation in adriamycin-induced cardiomyopathy in rats: effects of cardioprotective antioxidant. J Pineal Res, 26: 204-210.
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Year 2021, Volume: 4 Issue: 1, 1 - 15, 30.05.2021

Zeynep Erdoğmuş Özgen

https://doi.org/10.52538/iduhes.827754
Cited By: 1

Abstract

Project Number

YOK

References

  • Al-Majed, AA., Gado, AM., Al-Shabanah, OA., Mansour, MA.(2002). Alpha-lipoic acid ameliorates myocardial toxicity induced by Doksorubisin. Pharmacol Res,46:499-503.
  • Altieri, P., Spallarossa, P., Barisione, C., Garibaldi, S., Garuti, A., Fabbi, P., Ghigliotti, G., Brunelli, C.(2012). Inhibition of Doksorubisin-Induced Senescence by PPARδ Activation Agonists in Cardiac Muscle Cells: Cooperation between PPARδ and Bcl6. PLoS One, 7(9):e46126. doi: 10.1371/journal.pone.0046126.
  • Bates, SE., Rosing, DR., Lobins, RL.(2006). Challenges of evaluating the cardiac effects of anticancer agents. Clin Cancer Res, 12: 3871.
  • Berthiaume, J., Wallace, K. (2007). Adriamycin-induced oxidative mitochondrial cardiotoxicity. Cell Biol. Toxicol. 23, 15–25. Billingham, ME., Mason, JW., Bristow, MR., Daniels, JR.(1978). Antracycline cardiomyopathy monitered by morphologic changes. Cancer Treat Rep, 62: 865.
  • Bristow, M., Sageman, W.S, Scott, R.H., Billingham, M.E., Bowden, R.E., Kernoff, R.S., Snidow, I.H., Daniel, J.R.(1980). Acute and chronic cardiovascular effects of doxorubicin in the dog: The cardiovascular pharmacology of drug-induced histamine release. J. Cardiovasc. Pharmacol., 2; 487-515.
  • Carvalho, RA., Sousa, RP., Cadete, VJ., Lopaschuk, GD., Palmeira, CM., Bjork, JA. et al.(2010). Metabolic remodeling associated with subchronic doxorubicin cardiomyopathy. Toxicology, 270: 92–98.
  • Childs, A.C., Phaneuf, S. L., Dirks, A. J., Phillips, T., & Leeuwenburgh, C.(2002). Doxorubicin treatment in vivo causes cytochrome C release and cardiomyocyte apoptosis, as well as increased mitochondrial efficiency, superoxide dismutase activity, and Bcl-2: Bax ratio. Cancer research, 62(16), 4592-4598.
  • Cortes-Funes, H., Coronado C. ( 2007). Role of anthracyclines in the era of targeted therapy. Cardiovasc Toxicol, 7:56–60.
  • Cummings, J., Willmott, N., Smyth, J.(1991). The molecular pharmacology of doxorubicin in vivo. Eur J Cancer, 27: 532-535.
  • Deng, S., Kruger, A., Kleschyov, AL., Kalinowski, L., Daiber, A., Wojnowski, L.(2007). Gp91phox containing NAD(P)H oxidase increases superoxide formation by doxorubicin and NADPH. Free Radic Biol Med, 42: 466–473.
  • Deng, S., Yan, T., Jendrny, C., Nemecek, A., Vincetic, M., Gödtel-Armbrust, U., & Wojnowski, L. (2014). Dexrazoxane may prevent doxorubicin-induced DNA damage via depleting both topoisomerase II isoforms. BMC cancer, 14(1), 842.
  • Fogli, S., Nieri, P., Breschi, M.C. (2004). The role of nitric oxide in anthracycline toxicity and prospects for pharmacologic prevention of cardiac damage. FASEB J. 18,664–675.
  • Fridovich I.(1995). Superoxide radical and superoxide dismutases. Annu. Rev. Biochem.64, 97–112.
  • Galluzzi, L., Joza, N., Tasdemir, E., et al.(2009). No death without life: vital function of apoptotic effectors. Cell Death Differ, 16:1093–1107.
  • Gilleron, M., Marechal, X., Montaigne, D., Franczak, J., Neviere, R., Lancel, S.(2009). NADPH oxidases participate to doxorubicin-induced cardiac myocyte apoptosis. Biochem Biophys Res Commun, 388: 727–731.
  • Giorgio, M., Menna, P., Salvatorelli, E., Cairo, G., Gianni, L.(2004). Anthracyclines: Molecular Advances and Pharmacologic Developments in Antitumor Activity and Cardiotoxicity. Pharmacol Rev, 56:185-229.
  • Goffart, S., von Kleist-Retzow, J.-C., Wiesner, R.J.(2004). Regulation of mitochondrial proliferation in the heart: power-plant failure contributes to cardiac failure in hypertrophy. Cardiovasc. Res. 64, 198–207.
  • Goodman Gilman A. (2006). Goodman & Gilman's The Pharmacological Basis of Therapeutics. Eleventh edition. McGraw-Hill Medical Publishing Division, chapter: 51; 1358-1359.
  • Goormaghtigh, E., Chatelain, P., Caspers, J., Ruysschaert, JM.(1980). Evidence of a complex between adriamycin derivatives and cardiolipin: possible role in cardiotoxicity. Biochem Pharmacol, 29: 3003–3310.
  • Gu, J., Song, ZP., Gui, DM., Hu, W., Chen, YG., Zhang, DD.(2012). Resveratrol Attenuates Doksorubisin-Induced Cardiomyocyte Apoptosis in Lymphoma Nude Mice by Heme Oxygenase-1 Induction. Cardiovasc Toxicol., 12(4):341-349. Horenstein, MS., Vander Heide, RS., L'Ecuyer, TJ.(2000). Molecular basis of anthracyclineinduced cardiotoxicity and its prevention. Mol Genet Metab, 71: 436–444.
  • Huber, SA.(1990). Doxorubicin-induced alterations incultured myocardial cells stimulate cytolytic T-lymphocyte responses. Am J Pathol, 137: 449-456.
  • Ichikawa, Y., Ghanefar, M., Bayeva, M., Wu, R., Khechaduri, A., Prasad, S.V.N., Mutharasan, R.K., Naik, T.J., Ardehali, H. (2014). Cardiotoxicity of doxorubicin is mediated through mitochondrial iron accumulation. J. Clin. Investig. 124(2), 617-630.
  • Jain D. (2000). Cardiotoxicity of doxorubicin and other anthracycline derivatives. J Nucl Cardiol, 7: 53–62.
  • Janbabai, G., Nabati, M., Faghihinia, M., Azizi, S., Borhani, S., & Yazdani, J. (2017). Effect of enalapril on preventing anthracycline-induced cardiomyopathy. Cardiovascular toxicology, 17(2), 130-139.
  • Jordon, MA.(2002). Anti-cancer agents. Cur Med Chem, 2:1–17.
  • Kim, S. Y., Kim, S. J., Kim, B. J., Rah, S. Y., Chung, S. M., Im, M. J., & Kim, U. H. (2006). Doxorubicin-induced reactive oxygen species generation and intracellular Ca2+ increase are reciprocally modulated in rat cardiomyocytes. Experimental & Molecular Medicine, 38(5), 535-545.
  • L’Ecuyer T, Sanjeev S, Thomas R et al (2006) DNA damage is an early event in doxorubicin-induced cardiac myocyte death. Am J Physiol Heart Circ Physiol 291:H1273–H1280.
  • Lebrecht, D., Walker, UA. (2007). Role of mtDNA lesions in anthracycline cardiotoxicity. Cardiovasc Toxicol 7:108–113.
  • Li, J., Wang, P. Y., Long, N. A., Zhuang, J., Springer, D. A., Zou, J., ...&Hwang, P. M. (2019). p53 prevents doxorubicin cardiotoxicity independently of its prototypical tumor suppressor activities. Proceedings of the National Academy of Sciences, 116(39), 19626-19634.
  • Liu, B., Bai,, QX., Chen, XQ., Gao, GX., Gu, HT.(2007). Effect of curcumin on expression of survivin, Bcl-2 and Bax in human multiple myeloma cell line. Zhongguo Shi Yan Xue Ye Xue Za Zhi, 15: 762–766.
  • Ma, J., Wang, Y., Zheng, D., Wei, M., Xu, H., Peng, T.(2013). Rac1 signalling mediates Doksorubisin-induced cardiotoxicity through both reactive oxygen species-dependent and-independent pathways. Cardiovasc Res, 1;97(1):77-87.
  • Minotti, G., Recalcati, S., Menna, P., et al.(2004). Doxorubicin cardiotoxicity and the control of iron metabolism: quinone-dependent and independent mechanisms. Methods Enzymol, 378: 340-361.
  • Moens, AL., Leyton-Mange, JS., Niu, X., Yang, R., Cingolani, O., Arkenbout, EK. et al.(2009). Adverse ventricular remodeling and exacerbated NOS uncoupling from pressure-overload in mice lacking the beta3-adrenoreceptor. J Mol Cell Cardiol, 47: 576–585.
  • Morishima, I., Okumura, K., Matsui, H. et al. (1999). Zinc accumulation in adriamycin-induced cardiomyopathy in rats: effects of cardioprotective antioxidant. J Pineal Res, 26: 204-210.
  • Mukhopadhyay, P., Rajesh, M., Bátkai, S., Kashiwaya, Y., Hasko, G., Liaudet, L., ... & Pacher, P. (2009). Role of superoxide, nitric oxide, and peroxynitrite in doxorubicin-induced cell death in vivo and in vitro. American Journal of Physiology-Heart and Circulatory Physiology, 296(5), H1466-H1483.
  • Nabati, M., Janbabai, G., Baghyari, S., Esmaili, K., & Yazdani, J. (2017). Cardioprotective effects of carvedilol in inhibiting doxorubicin-induced cardiotoxicity. Journal of Cardiovascular Pharmacology, 69(5), 279-285.
  • Neilan, TG., Blake, SL., Ichinose, F., Raher, MJ., Buys, ES., Jassal, DS.(2007). Disruption of nitric oxide synthase 3 protects against the cardiac injury, dysfunction, and mortality induced by doxorubicin. Circulation, 116: 506–514.
  • Nishiyama, K., Yasue, H., Moriyama, Y. et al.(2001). Acute effects of melatonin administration on cardiovascular autonomic regulation in healty men. Am Heart J, 141: 149.
  • Nitobe, J., Yamaguchi, S., Okuyama, M., Nozaki, N., Sata, M., Miyamoto, T., et al. (2003). Reactive oxygen species regulate FLICE inhibitory protein (FLIP) and susceptibility to Fas mediated apoptosis in cardiac myocytes. Cardiovasc Res, 57: 119–128.
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Details

Primary Language Turkish
Subjects Pharmacology and Pharmaceutical Sciences
Journal Section Articles
Authors

Zeynep Erdoğmuş Özgen 0000-0001-6607-836X

Project Number YOK
Publication Date May 30, 2021
Submission Date November 18, 2020
Published in Issue Year 2021 Volume: 4 Issue: 1

Cite

APA Erdoğmuş Özgen, Z. (2021). DOKSORUBİSİN KARDİYOTOKSİSİTESİNİN OLUŞUMU VE ÖNLENMESİ. Izmir Democracy University Health Sciences Journal, 4(1), 1-15. https://doi.org/10.52538/iduhes.827754

Cited By

DOKSORUBİSİN İLE OLUŞTURULAN BÖBREK HASARINDA LERKANİDİPİNİN ANTİOKSİDAN VE ANTİAPOPTOTİK ETKİLERİNİN BCL-2/BAX/SİT C/ CAS-3 YOLAĞI ÜZERİNDEN ARAŞTIRILMASI
SDÜ Tıp Fakültesi Dergisi
https://doi.org/10.17343/sdutfd.1198304
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