Oxidative and non-oxidative mechanisms in the inactivation of cardiac mitochondrial electron transport chain components by doxorubicin
Population
Bovine heart submitochondrial preparations (SMP)
Design
Preclinical
Follow-up
15 min to 2 h (in vitro incubation)
Authors
Discussion
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Member takes
Implication
May guide targeted antioxidant strategies in anthracycline cardiotoxicity models; leaves open clinical translation from this animal study.
Structured PICO
P
Population
Bovine heart submitochondrial preparations (SMP)
I
Intervention
Doxorubicin (25-50 microM and 0.5-1.0 mM)
O
Outcome
Inactivation of cardiac mitochondrial electron transport chain components (NADH dehydrogenase, NADH oxidase, succinate dehydrogenase, succinate oxidase, cytochrome c oxidase)surrogate
Doxorubicin causes cardiotoxicity through both oxidative and non-oxidative mechanisms depending on concentration, with low concentrations causing site-specific oxidative damage to the NADH oxidation pathway.
Cite This Study
Marcillat et al. (1989) studied this question.