Title:Anthracycline in Medicinal Chemistry: Mechanism of Cardiotoxicity, Preventive and
Treatment Strategies
Volume: 27
Issue: 4
Author(s): Narmin Hamaamin Hussen, Aso Hameed Hasan*, Gashbeen Osman Muhammed, Akar Yousif Yassin, Roza Rafiq Salih, Parwa Ahmed Esmail, Mohammed M. Alanazi and Joazaizulfazli Jamalis
Affiliation:
- Department of Chemistry, College of Science, University of Garmian, Kalar, 46021, Kurdistan Region-Iraq, Iraq
- Department
of Chemistry, Faculty of Science, Universiti Teknologi Malaysia, 81310 Johor, Bahru, Johor, Malaysia
Keywords:
Anthracycline, cardiotoxicity, reactive oxygen species, secondary alcohol metabolite, prevention, treatment.
Abstract: Anthracyclines are one of the most effective cancer treatments ever created, but
these compounds are somewhat cardiotoxic to some patients, causing heart failure. The likelihood
of such adverse effects restricts the overall prescribed dose of anthracyclines for patients.
Based on the pathophysiology of anthracycline-induced cardiotoxicity, the cardiotoxicity
plausibly originates from a reduction reaction of a single electron in its structure to form
surplus reactive oxygen species (ROS) or two electrons reducing and converting into C-13
alcohol metabolites. While excess ROS is the probable cause for acute cardiotoxicity brought
on by anthracyclines, it is not all characteristic of progressive cardiomyopathy. The formed
secondary alcohol metabolites could also profoundly accelerate cardiotoxicity, which then
develops into cardiomyopathy and eventually congestive heart failure. This review offers an
overview of the molecular pathways of anthracycline-induced cardiotoxicity, emphasizing the roles of secondary
alcohol metabolites of anthracyclines and/or their morbific role as ROS. The most effective ways to minimize or
terminate anthracycline-induced cardiotoxicity are also covered.