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Microtubule‐Targeting Chemotherapy Causes Mitochondrial Dysfunction in Heart and Skeletal Muscle

A variety of chemotherapies are associated with muscle dysfunction but the mechanisms are poorly understood. Emerging evidence suggests doxorubicin (DNA targeted chemotherapy) impairs mitochondrial respiration and increases H2O2 emission. However, whether other chemotherapies create similar mitochondrial dysfunctions in muscle is unknown. An emerging model proposes that microtubules can inhibit mitochondrial ADP import/ATP export by blocking outer membrane voltage‐dependent anion channels (VDAC). We hypothesized that microtubule‐targeting chemotherapies (taxol, microtubule stabilizer; vinblastine, microtubule destabilizer) may alter ADP control of oxidative phosphorylation by changing VDAC‐permeability to ADP. We also hypothesized that these chemotherapies would alter mitochondrial H2O2 emission considering ADP suppresses H2O2 emission from mitochondria during oxidative phosphorylation.