The use of serum levels of cardiac troponin T to compare the protective activity of dexrazoxane against doxorubicin- and mitoxantrone-induced cardiotoxicity

Herman, Eugene H.; Zhang, Jun; Rifai, Nader; Lipshultz, Steven E.; Hasinoff, Brian B.; Chadwick, D. P.; Knapton, Alan; Chai, Jonathan; Ferrans, Víctor J.

doi:10.1007/s002800100348

Cited by 93 publications

(68 citation statements)

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“…The mechanism of MITO-induced cardiotoxicity is probably similar to that of other anthracyclines [18][19][20]. There are limited experimental studies on MITO-induced cardiotoxicity [6,7,19,21,22], but we did not find any experimental study in the literature on the cardioprotective effects of AMI against MITO-induced acute cardiotoxicity.…”

Section: Introductioncontrasting

confidence: 40%

“…Doxorubicin can cause edema, cytoplasmic vacuolization, degeneration, myofibrillar loss, inflammation, apoptosis, and fibrosis in cardiomyocytes [13,14,21,22]. Billingham's score was higher than in controls in the evaluation of chronic doxorubicin cardiotoxicity in two studies [14,21].…”

Section: Discussionmentioning

confidence: 99%

“…The cumulative doses were 2.4-7.2 mg/kg [20][21][22][23]. However, there is no study with the exception of cell culture on MITOinduced acute cardiotoxicity in rats.…”

Section: Animals and Treatment Protocolsmentioning

confidence: 99%

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The protection of the myocardium by amifostine against mitoxantrone-induced acute cardiotoxicity in rats

Kadıköylü¹,

Meteoğlu²,

Demi̇r³

et al. 2010

Turk J Hematol

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Objective: Amifostine (AMI) has been used for the prevention of doxorubicin-induced cardiotoxicity in several experimental and a few clinical studies. The aim of this study was to investigate the effects of AMI on lipid peroxidation, protective enzymes, and mitoxantrone (MITO)-induced acute cardiotoxicity in the rat heart using biochemical tests and histopathological examinations. Materials and Methods: Thirty-six rats were divided into six groups (n=6 in each). Control rats were given intraperitoneal (i.p.) serum saline and AMI group rats were given 200 mg/kg AMI i.p. Rats received MITO-2.5 and 5 mg/kg i.p. in the MITO-2.5 and MITO-5 groups. AMI 200 mg/kg i.p. was administered 30 min. before the same doses of MITO in the MITO-2.5+AMI and MITO-5+AMI groups. Results: The levels of cardiac enzymes such as creatinine phosphokinase-myocardial band and cardiac troponin T did not change. Malondialdehyde (MDA) levels increased in MITO groups compared to controls. Catalase and glutathione (GSH) levels in the MITO and MITO+AMI groups were higher than in controls. Superoxide dismutase and glutathione peroxidase levels were not different between MITO groups and controls. There was no difference in MDA levels between MITO+AMI groups and controls. Calcium deposition was not detected. The scores of fibrosis, apoptosis, inflammation, and degeneration in MITO groups were higher than in controls. The scores of fibrosis, degeneration and inflammation in MITO+AMI groups were lower. Conclusion: MITO caused lipid peroxidation and myocardial damage, and the myocardium increased catalase and GSH levels to prevent this damage. AMI can protect against MITO-induced acute cardiotoxicity, decreasing myocardial damage and lipid peroxidation. (Turk J Hematol 2010; 27: 62-9)

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Section: Introductioncontrasting

confidence: 40%

Section: Discussionmentioning

confidence: 99%

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The protection of the myocardium by amifostine against mitoxantrone-induced acute cardiotoxicity in rats

Kadıköylü¹,

Meteoğlu²,

Demi̇r³

et al. 2010

Turk J Hematol

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“…Furthermore, animal data revealed that the combination of mitoxantrone with the cardioprotector dexrazoxane may be useful to ameliorate, or even prevent, the mitoxantroneassociated cardiotoxicity. [37][38][39] Interestingly, dexrazoxane was shown to increase the efficacy of mitoxantrone in experimental autoimmune encephalomyelitis. 39 An alternative would be the development of other anthracenedione derivatives with lower cardiotoxicity.…”

Section: Adverse Effectsmentioning

confidence: 99%

Immunosuppressive Agents in Multiple Sclerosis

2007

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Summary:Immunosuppressive agents have been used in multiple sclerosis (MS) for decades. The approval of several immunomodulatory agents against MS beginning in the 1990s, whose putative mechanisms of action appeared "more MSspecific," curtailed the importance of immunosuppressants, which made them treatment options of second choice. However, with the recent approval of mitoxantrone for treatment of patients with active forms of relapsing-remitting or secondary progressive MS and with a number of oral immunosuppressive agents being assessed in phase II and III clinical trials, a "renaissance" of this type of agents is currently occurring. This review provides an outline of the most important clinical studies and discusses relevant side effects of the major immunosuppressants (i.e., mitoxantrone, azathioprine, cyclophosphamide, methotrexate, mycophenolate mofetil, cladribine, and sirolimus/temsirolimus). The current knowledge of the putative mechanisms of action of these compounds is discussed.

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“…Preus et al [9] reported the usefulness of LDH-1, LDH-2, and CK-MB, while various other authors reported troponin I and/or troponin T as markers for myocardial damage in rats [1,2,4,5,8,12]. Recently, the International Life Science Institute (ILSI) / Health Environmental Science Institute (HESI) have undertaken a comprehensive study focusing on the influence of methodological differences regarding troponin I detection in diluted samples of serum from rats treated with isoproterenol.…”

mentioning

confidence: 99%

Correlation among Clinicopathological Parameters of Myocardial Damage in Rats Treated with Isoproterenol

et al. 2007

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Abstract:The correlation among clinicopathological parameters of myocardial damage was investigated in rats administered a single subcutaneous dose of isoproterenol at 0 (saline), 0.04, 0.4 and 4 mg/kg. Total lactate dehydrogenase (LDH), creatine kinase (CK), and their isoenzymes (LDH-1, LDH-2 and CK-MB), as well as troponin I and tropinin T, were measured 4 h after the administration of the drug. Troponin I was determined by a chemiluminescence method using Bayer Centaur and DPC Immulyze, as well as by ELISA. Troponin T was assayed semi-quantitatively using Trop T Sensitive. A high correlation was found among LDH isoenzymes, troponin I (Centaur) and troponin T. The present result provides a baseline for interpreting changes in the different parameters of myocardial damage assayed by different methods in toxicity studies.

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The use of serum levels of cardiac troponin T to compare the protective activity of dexrazoxane against doxorubicin- and mitoxantrone-induced cardiotoxicity

Abstract: The present study showed that DRZ significantly attenuates the cardiotoxicity induced by DXR and MTX, and that this protective activity can be assessed by morphological evaluation of cardiac tissues and by monitoring the concentrations of cTnT in serum.

Cited by 93 publications

References 0 publications

The protection of the myocardium by amifostine against mitoxantrone-induced acute cardiotoxicity in rats

The protection of the myocardium by amifostine against mitoxantrone-induced acute cardiotoxicity in rats

Immunosuppressive Agents in Multiple Sclerosis

Correlation among Clinicopathological Parameters of Myocardial Damage in Rats Treated with Isoproterenol

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