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- W3176646721 abstract "Debilitating muscle weakness and fatigue are common side effects of chemotherapy in cancer patients, limiting recovery and increasing morbidity. Our previous work shows that doxorubicin, a common chemotherapy drug, elevates reactive oxygen species (ROS) and decreases contractile force in skeletal muscle. As mitochondria represent a primary source of oxidant generation in muscle, we hypothesized that doxorubicin may compromise mitochondrial respiratory control and increase ROS production. 72 hrs following a single doxorubicin injection (20 mg/kg), maximal ADP-stimulated O2 consumption was decreased during respiration supported by palmitoylcarnitine (PC) (−46 ± 26 %, p<0.05) and pyruvate/malate (−43 ± 21 %, p<0.05, n=6/group) in permeabilized fiber bundles (PmFB) from red gastrocnemius muscle. PmFB from doxorubicin treated animals also display increased rates of mitochondrial H2O2 emission with PC (23 ± 2 %) and 3-phosphoglycerate (49 ± 2 %, p=0.1). Our data indicate that doxorubicin impairs both maximal State 3, and fatty-acid-supported respiration. In addition, doxorubicin promotes mitochondrial ROS generation, a potential underlying cause of doxorubicin-induced muscle dysfunction. Supported by DK073488" @default.
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- W3176646721 date "2012-04-01" @default.
- W3176646721 modified "2023-10-16" @default.
- W3176646721 title "Doxorubicin impairs skeletal muscle mitochondrial respiratory capacity in skeletal muscle" @default.
- W3176646721 doi "https://doi.org/10.1096/fasebj.26.1_supplement.1144.8" @default.
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