Taurine rescues cisplatin-induced muscle atrophy in vitro: a morphological study

Cisplatin (CisPt) is a widely used chemotherapeutic drug whose side-effectsinclude muscle weakness and cachexia. Here we analysed CisPt-induced atrophy in C2C12 myotubes by a multidisciplinary morphological approach, focusing on the onset and progression of autophagy, a protective cellular process that, when excessively activated, may trigger protein hypercatabolism and atrophy in skeletal muscle. To visualize autophagy we used confocal and transmission electron microscopy at different times of treatment and doses of CisPt. As well we evaluated the effects of Taurine, a cytoprotective beta-amino acid able to counteract oxidative stress, apoptosis and endoplasmic reticulum stress in different tissues and organs. Our microscopic results indicate that autophagy occurs very early in 50microM CisPt challenged myotubes (4h-8h) before overt atrophy but it persists even at 24h, when several autophagic vesicles, damaged mitochondria and sarcoplasmic blebbings engulfe the sarcoplasm. Differently, 25microM Taurine pre-treatment rescues the majority of myotubes size upon 50 microM CisPt at 24h. Taurine appears to counteract atrophy by restoring regular microtubular apparatus, mitochondria, and reducing the overload and the localization of auto phagolysosomes. Such a promising Taurine action in preventing atrophy needs further molecular and biochemical studies to best define its impact on muscle homeostasis and the maintenance of an adequate skeletal mass in vivo.