Chemotherapy linked to mitochondrial dysfunction in skeletal muscle

A study published in the American Journal of Physiology-Cell Physiology has found that chemotherapy can cause adverse effects on the skeletal muscle of patients undergoing treatment. In the study, researchers from the University of Vermont looked at whether chemotherapeutics for breast cancer impact skeletal muscle structure and protein expression.

• The researchers involved 13 women diagnosed with breast cancer and undergoing chemotherapy as part of their initial treatment after tumor resection. In addition, 12 healthy women took part as nondiseased controls.
• An examination of those with breast cancer revealed reduced single-muscle fiber cross-sectional area and fractional content of subsarcolemmal and intermyofibrillar mitochondria.
• The patients who had received chemotherapeutic drugs, in particular, doxorubicin and paclitaxel exhibited reductions in myosin expression, mitochondrial loss, and increased reactive oxygen species (ROS) production in C2C12 murine myotube cell cultures. This supported initial findings on the role of chemotherapy in atrophic and mitochondrial phenotypes.
• After the patients were treated with mitochondrial-targeted antioxidant MitoQ, researchers noted a drop in chemotherapy-induced myosin depletion, mitochondrial loss, and ROS production.
• Patients who underwent chemotherapy also exhibited increased levels of peroxiredoxin 3, a mitochondrial peroxidase linked to reductions in muscle fibers.

Researchers concluded that chemotherapy can negatively affect skeletal muscle in patients undergoing therapy.

Learn more about the negative effects of chemotherapy at Chemotherapy.news.

Journal Reference:

Guigni BA, Callahan DM, Tourville TW, Miller MS, Fiske B, Voigt T, Korwin-Mihavics B, Anathy V, Dittus K, Toth MJ. Skeletal muscle atrophy and dysfunction in breast cancer patients: role for chemotherapy-derived oxidant stress. American Journal of Physiology-Cell Physiology. November 2018;315(5). DOI: 10.1152/ajpcell.00002.2018