The cytotoxicity of celecoxib towards cardiac myocytes is cyclooxygenase-2 independent

Cardiovascular Toxicology

Volumn 7, Issue 1, 2007, Pages 19-27

  Hasinoff, Brian B ^a   Patel, Daywin ^a   Wu, Xing ^a  

^a UNIVERSITY OF MANITOBA   (Canada)

Author keywords

Apoptosis; Celecoxib; COX 2; Cyclooxygenase Myocyte; Cytotoxicity; Iloprost; Rofecoxib

Indexed keywords

CASPASE 3; CASPASE 7; CELECOXIB; CYCLOOXYGENASE 2; DICHLOROFLUORESCEIN; DOXORUBICIN; ILOPROST; LACTATE DEHYDROGENASE; PROSTACYCLIN; REACTIVE OXYGEN METABOLITE; ROFECOXIB;

ANIMAL EXPERIMENT; APOPTOSIS; ARTICLE; CONTROLLED STUDY; CYTOTOXICITY; DRUG MECHANISM; ENZYME ACTIVITY; HEART MUSCLE CELL; NONHUMAN; OXIDATION; PRIORITY JOURNAL; RAT;

ANIMALS; ANIMALS, NEWBORN; ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL; CELL DEATH; CELL LINE; CELL PROLIFERATION; CELLS, CULTURED; CYCLOOXYGENASE 2; CYCLOOXYGENASE 2 INHIBITORS; FLUORESCENT DYES; HUMANS; ILOPROST; K562 CELLS; L-LACTATE DEHYDROGENASE; LACTONES; MICROSCOPY, FLUORESCENCE; MYOCYTES, CARDIAC; PLATELET AGGREGATION INHIBITORS; PYRAZOLES; RATS; RATS, SPRAGUE-DAWLEY; SULFONAMIDES; SULFONES;

RATTUS;

EID: 34548315729     PISSN: 15307905     EISSN: None     Source Type: Journal    
DOI: 10.1007/s12012-007-0002-8     Document Type: Article

References (29)

1. Adderley, S. R., & Fitzgerald, D. J. (1999). Oxidative damage of cardiomyocytes is limited by extracellular regulated kinases 1/2-mediated induction of cyclooxygenase-2. The Journal of Biological Chemistry, 274, 5038-5046.
2. Barnabé, N., Butler, M., & Hasinoff, B. B. (2001). The effect of the catalytic topoisomerase II inhibitor dexrazoxane (ICRF-187) on CC9C10 hybridoma viability and productivity. Cytotechnology, 37, 107-117.
3. Billingham, M., & Bristow, M. (1984). Evaluation of anthracycline cardiotoxicity: Predictive ability and functional correlation of endomycardial biopsy. Cancer Treatment Symposia, 3, 71-76.
4. Brooks, G., Poolman, R. A., & Li, J. M. (1998). Arresting developments in the cardiac myocyte cell cycle: Role of cyclin-dependent kinase inhibitors. Cardiovascular Research, 39, 301-311.
5. Chan, C. C., Boyce, S., Brideau, C., Charleson, S., Cromlish, W., Ethier, D., Evans, J., Ford-Hutchinson, A. W., Forrest, M. J., Gauthier, J. Y., Gordon, R., Gresser, M., Guay, J., Kargman, S., Kennedy, B., Leblanc, Y., Leger, S., Mancini, J., O'Neill, G. P., Ouellet, M., Patrick, D., Percival, M. D., Perrier, H., Prasit, P., Rodger, I., et al. (1999). Rofecoxib [Vioxx, MK-0966; 4-(4′-methylsulfonylphenyl)-3-phenyl-2-(5H)-furanone]: A potent and orally active cyclooxygenase-2 inhibitor. Pharmacological and biochemical profiles. The Journal of Pharmacology and Experimental Therapeutics, 290, 551-560.
6. Cocco, T., Di Paola, M., Papa, S., & Lorusso, M. (1999). Arachidonic acid interaction with the mitochondrial electron transport chain promotes reactive oxygen species generation. Free Radical Biology and Medicine, 27, 51-59.
7. Davies, N. M., McLachlan, A. J., Day, R. O., & Williams, K. M. (2000). Clinical pharmacokinetics and pharmacodynamics of celecoxib: A selective cyclo-oxygenase-2 inhibitor. Clinical Pharmacokinetics, 38, 225-242.
8. Davies, N. M., Teng, X. W., & Skjodt, N. M. (2003). Pharmacokinetics of rofecoxib: A specific cyclo-oxygenase-2 inhibitor. Clinical Pharmacokinetics, 42, 545-556.
9. Dowd, N. P., Scully, M., Adderley, S. R., Cunningham, A. J., & Fitzgerald, D. J. (2001). Inhibition of cyclooxygenase-2 aggravates doxorubicin-mediated cardiac injury in vivo. The Journal of Clinical Investigation, 108, 585-590.
10. Fosslien, E. (2005). Cardiovascular complications of non-steroidal anti-inflammatory drugs. Annals of Clinical and Laboratory Science, 35, 347-385.
11. Gabizon, A. A., Lyass, O., Berry, G. J., & Wildgust, M. (2004). Cardiac safety of pegylated liposomal doxorubicin (Doxil/Caelyx) demonstrated by endomyocardial biopsy in patients with advanced malignancies. Cancer Investigation, 22, 663-669.
12. Grosser, T., Fries, S., & FitzGerald, G. A. (2006). Biological basis for the cardiovascular consequences of COX-2 inhibition: therapeutic challenges and opportunities. The Journal of Clinical Investigation, 116, 4-15.
13. Hasinoff, B. B., Abram, M. E., Barnabé, N., Khelifa, T., Allan, W. P., & Yalowich, J. C. (2001). The catalytic DNA topoisomerase II inhibitor dexrazoxane (ICRF-187) induces differentiation and apoptosis in human leukemia K562 cells. Molecular Pharmacology, 59, 453-461.
14. Hasinoff, B. B., Abram, M. E., Chee, G.-L., Huebner, E., Byard, E. H., Barnabé, N., Ferrans, V. J., Yu, Z.-X., & Yalowich, J. C. (2000). The catalytic DNA topoisomerase II inhibitor dexrazoxane (ICRF-187) induces endopolyploidy in Chinese hamster ovary cells. The Journal of Pharmacology and Experimental Therapeutics, 295, 474-483.
15. Hasinoff, B. B., Patel, D., & Wu, X. (2003). The oral iron chelator ICL670A (deferasirox) does not protect myocytes against doxorubicin. Free Radical Biology and Medicine, 35, 1469-1479.
16. Kearney, P. M., Baigent, C., Godwin, J., Halls, H., Emberson, J.R., & Patrono, C. (2006). Do selective cyclo-oxygenase-2 inhibitors and traditional non-steroidal anti-inflammatory drugs increase the risk of atherothrombosis? Meta-analysis of randomised trials. British Medical Journal, 332, 1302-1308.
17. Knudsen, J. F., Carlsson, U., Hammarstrom, P., Sokol, G. H., & Cantilena, L. R. (2004). The cyclooxygenase-2 inhibitor celecoxib is a potent inhibitor of human carbonic anhydrase II. Inflammation, 28, 285-290.
18. Li, F., Wang, X., Capasso, J. M., & Gerdes, A. M. (1996). Rapid transition of cardiac myocytes from hyperplasia to hypertrophy during postnatal development. Journal of Molecular and Cell Cardiology, 28, 1737-1746.
19. Lim, C. C., Zuppinger, C., Guo, X., Kuster, G. M., Helmes, M., Eppenberger, H. M., Suter, T. M., Liao, R., & Sawyer, D. B. (2004). Anthracyclines induce calpain-dependent titin proteolysis and necrosis in cardiomyocytes. The Journal of Biological Chemistry, 279, 8290-8299.
20. Lin, H. P., Kulp, S. K., Tseng, P. H., Yang, Y. T., Yang, C. C., & Chen, C. S. (2004). Growth inhibitory effects of celecoxib in human umbilical vein endothelial cells are mediated through G1 arrest via multiple signaling mechanisms. Molecular Cancer Therapeutics, 3, 1671-1680.
21. Maier, T. J., Schilling, K., Schmidt, R., Geisslinger, G., & Grosch, S. (2004). Cyclooxygenase-2 (COX-2)-dependent and -independent anticarcinogenic effects of celecoxib in human colon carcinoma cells. Biochemical Pharmacology, 67, 1469-1478.
22. Mitchell, J. A., & Warner, T. D. (2006). COX isoforms in the cardiovascular system: Understanding the activities of non-steroidal anti-inflammatory drugs. Nature Reviews Drug Discovery, 5, 75-86.
23. O'Connell, T. D., Berry, J. E., Jarvis, A. K., Somerman, M. J., & Simpson, R. U. (1997). 1,25-Dihydroxyvitamin D3 regulation of cardiac myocyte proliferation and hypertrophy. The American Journal of Physiology, 272, H1751-H1758.
24. O'Malley, Y. Q., Reszka, K. J., & Britigan, B. E. (2004). Direct oxidation of 2′,7′-dichlorodihydrofluorescein by pyocyanin and other redox-active compounds independent of reactive oxygen species production. Free Radical Biology and Medicine, 36, 90-100.
25. Solomon, S. D., McMurray, J. J., Pfeffer, M. A., Wittes, J., Fowler, R., Finn, P., Anderson, W.F., Zauber, A., Hawk, E., & Bertagnolli, M. (2005). Cardiovascular risk associated with celecoxib in a clinical trial for colorectal adenoma prevention. The New England Journal of Medicine, 352, 1071-1080.
26. Subhashini, J., Mahipal, S. V., & Reddanna, P. (2005). Anti-proliferative and apoptotic effects of celecoxib on human chronic myeloid leukemia in vitro. Cancer Letters, 224, 31-43.
27. Tong, Z., Wu, X., Chen, C. S., & Kehrer, J. P. (2006). Cytotoxicity of a non-cyclooxygenase-2 inhibitory derivative of celecoxib in non-small-cell lung cancer A549 cells. Lung Cancer, 52, 117-124.
28. Wang, D., Wang, M., Cheng, Y., & Fitzgerald, G. A. (2005). Cardiovascular hazard and non-steroidal anti-inflammatory drugs. Current Opinion in Pharmacology, 5, 204-210.
29. Zhang, G. S., Liu, D. S., Dai, C. W., & Li, R. J. (2006). Anti-tumor effects of celecoxib on K562 leukemia cells are mediated by cell-cycle arrest, caspase-3 activation, and downregulation of Cox-2 expression and are synergistic with hydroxyurea or imatinib. American Journal of Hematology, 81, 242-255.