Key result
Adriamycin-Fe3+ caused inactivation of rat heart mitochondrial creatine kinase due to oxidative damage of sulfhydryl groups associated with lipid peroxidation.
Population
Rat heart mitochondria
Comparison
Adriamycin (ADM)-Fe3+ exposure vs Various antioxidants and radical scavengers
Design
Preclinical
Authors
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Supports oxidative mechanisms in anthracycline cardiotoxicity models; leaves open human relevance pending clinical studies.
Adriamycin-Fe3+ inactivates rat heart mitochondrial creatine kinase through oxidative damage of sulfhydryl groups linked to lipid peroxidation, providing insight into doxorubicin-induced cardiotoxicity mechanisms.
Miura et al. (1994) studied Adriamycin-induced lipid peroxidation. Adriamycin (ADM)-Fe3+ was evaluated on Inactivation of rat heart mitochondrial creatine kinase (CK) and lipid peroxidation. Adriamycin-Fe3+ caused inactivation of rat heart mitochondrial creatine kinase due to oxidative damage of sulfhydryl groups associated with lipid peroxidation.
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