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Effect of methimazole treatment on doxorubicin-induced cardiotoxicity in mice
Abdel-Moneim M Osman1, Marwa M Nemnem, Amany A Abou-Bakr
1College of Medicine, Pharmacology Dept, King Abdel-Aziz University, Jeddah, Saudi Arabia. moneimosman@hotmail.com
Abstract:
The major limiting factor in long-term administration of doxorubicin is the development of cumulative dose-dependent cardiomyopathy and congestive heart failure that limit the use of this drug. The present study was undertaken to find out the chemo protective role of methimazole against doxorubicin-induced cardiotoxicity in experimental animals. In the present study, doxorubicin treatment in a dose of 3mg/kg, i.p., every other day for six doses showed a significant 2.6-, 3- and 10.5-fold increase in the cardiac enzyme activities CK-MB and LDH and troponin-I, respectively, in the serum of the animals. Histopathological investigation of heart tissues showed swollen muscle fibers with interstitial edema and inflammatory exudate. Pretreatment of the animals with methimazole at a dose level of 40 mg/kg, i.p., 30 min before doxorubicin, returned the cardiac enzyme levels to nearly normal value with partial reversal of the inflammatory lesions and the swollen muscle fibers induced by doxorubicin. Moreover, methimazole pretreatment, decreased the doxorubicin level in the heart tissues with a significant increase in plasma level and non significant effect on doxorubicin level in tumor cells. At the same time, methimazole pretreatment did not significantly interfere with the antitumor activity of doxorubicin.
Insights
Methimazole offers a protective effect against doxorubicin-induced cardiotoxicity in animal models. This chemoprotective agent reduced cardiac enzyme levels and improved heart tissue damage without compromising doxorubicin
Area of Science:
- Cardiology
- Pharmacology
- Oncology
Background:
- Doxorubicin is a widely used chemotherapy agent.
- Cardiotoxicity, including cardiomyopathy and congestive heart failure, limits its long-term use.
- Developing strategies to mitigate doxorubicin-induced cardiotoxicity is crucial.
Purpose of the Study:
- To investigate the cardioprotective potential of methimazole against doxorubicin-induced cardiotoxicity.
- To evaluate the effect of methimazole on cardiac enzyme levels and heart tissue histology in an animal model.
Main Methods:
- Experimental animals were treated with doxorubicin (3 mg/kg, i.p., every other day for six doses).
- Cardiac enzyme activities (CK-MB, LDH, troponin-I) and doxorubicin levels in heart and plasma were measured.
- Histopathological examination of heart tissues was performed.
- Animals were pretreated with methimazole (40 mg/kg, i.p.) 30 minutes prior to doxorubicin administration.
Main Results:
- Doxorubicin treatment significantly increased serum cardiac enzyme activities (CK-MB, LDH, troponin-I) and caused histopathological damage.
- Methimazole pretreatment normalized cardiac enzyme levels and partially reversed inflammatory lesions and muscle fiber swelling.
- Methimazole decreased doxorubicin concentration in heart tissue while increasing it in plasma.
- Methimazole did not significantly affect the antitumor activity of doxorubicin.
Conclusions:
- Methimazole demonstrates significant cardioprotective effects against doxorubicin-induced cardiotoxicity in experimental animals.
- Methimazole mitigates doxorubicin-induced cardiac damage by reducing drug accumulation in the heart.
- Methimazole represents a promising therapeutic strategy to improve the safety profile of doxorubicin chemotherapy.
