Key result
Doxorubicin treatment in rats led to early down-regulation of NADH:quinone oxidoreductase-1 activity and increased hydrogen peroxide production by NADPH oxidases.
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Does not support changes in doxorubicin use; leaves open NQO1 as a therapeutic target in humans.
CONTEXT: Doxorubicin cardiotoxicity displays a complex and multifactorial progression. OBJECTIVE: Identify early biochemical mechanisms leading to a sustained imbalance of cellular bioenergetics. METHODS: Measurements of the temporal evolution of selected biochemical markers after treatment of rats with doxorubicin (20 mg/kg body weight). RESULTS: Doxorubicin treatment increased lipid oxidation, catalase activity and production of H₂O₂ by Nox-NADPH oxidases, and down-regulated NAD(P)H: quinone oxidoreductase-1 prior eliciting changes in reduced glutathione, protein carbonyls and protein nitrotyrosines. Alterations of mitochondrial and myofibrillar bioenergetics biomarkers were detected only after this oxidative imbalance was established. NAD(P)H: quinone oxidoreductase-1 activity and increase of hydrogen peroxide production by NADPH oxidases are early biomarkers in doxorubicin cardiotoxicity.
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Lagoa et al. (2014) studied Doxorubicin cardiotoxicity. Doxorubicin was evaluated on Temporal evolution of selected biochemical markers. Doxorubicin treatment in rats led to early down-regulation of NADH:quinone oxidoreductase-1 activity and increased hydrogen peroxide production by NADPH oxidases.
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