College of Health & Biomedicine, Victoria University, Melbourne, Victoria, Australia; Institute of Sport, Exercise & Active Living, Victoria University, Melbourne, Victoria, Australia; Australian Institute for Musculoskeletal Science, Melbourne, Victoria, Australia.
College of Health & Biomedicine, Victoria University, Melbourne, Victoria, Australia; Institute of Sport, Exercise & Active Living, Victoria University, Melbourne, Victoria, Australia; Australian Institute for Musculoskeletal Science, Melbourne, Victoria, Australia.
Mitochondrion. 2018 Sep;42:33-49. doi: 10.1016/j.mito.2017.10.010. Epub 2017 Oct 25.
Chemotherapeutic agents (CAs) can independently promote skeletal muscle dysfunction, fatigue and wasting with mitochondrial toxicity implicated as a possible mechanism. Thus, we aimed to characterise the effects of various CAs on mitochondrial function, viability and oxidant production in C2C12 myoblasts and myotubes. All CAs significantly reduced the viable mitochondrial pool but did not affect mitochondrial functional parameters. Doxorubicin and oxaliplatin increased oxidant production in myotubes while all CAs, except for irinotecan, increased oxidant production in myoblasts and reduced myotube diameter. Our data demonstrate CAs mito-toxic effects, highlighting the potential for mitochondria-protective therapeutics to address chemotherapy-induced skeletal muscle damage.
化疗药物（CAs）可独立促进骨骼肌功能障碍、疲劳和消耗，线粒体毒性被认为是一种可能的机制。因此，我们旨在研究各种 CAs 对 C2C12 成肌细胞和肌管中线粒体功能、活力和氧化剂产生的影响。所有 CAs 均显著降低了有活力的线粒体池，但不影响线粒体功能参数。阿霉素和奥沙利铂增加了肌管中的氧化剂产生，而除伊立替康外，所有 CAs 均增加了成肌细胞中的氧化剂产生并减少了肌管直径。我们的数据表明 CAs 具有线粒体毒性作用，强调了使用线粒体保护治疗来解决化疗引起的骨骼肌损伤的潜力。
