DOD

direct oxidative damage to cellular components remains a common postulated mechanism of

AIC, there are alternative proposed mechanisms that probably contribute to cardiac dysfunction.
Anthracycline compounds have a planar structure, which intercalates into the DNA through
noncovalent interaction, preventing further DNA and RNA synthesis and likely contributing to
the death of myocytes and mitochondrial mutations. Anthracyclines disrupt DNA by poisoning
topoisomerase, a critical enzyme for unwinding of the DNA for replication and synthesis,
thereby causing growth arrest and programmed cell death.