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Oxidative stress is one of the major players in initiating apoptotic cell death in skeletal muscle, contributing to mitochondria- mediated apoptotic signaling in several myopathies as well as in a variety of atrophic conditions. Melatonin, known as a free radical scavenger and able to stimulate anti-oxidant enzyme efficiency in different cell models, could provide protection against oxidative stress in skeletal muscle too. Here, melatonin effect has been investigated in C2C12 myoblasts, exposed to apoptotic chemical triggers which lead to radical oxygen species increase. Cells were treated with melatonin before exposure to cisplatin or staurosporine and cell behavior investigated by means of cytometric and morpho-functional analyses. In myoblasts, melatonin prevents mitochondria damage and apoptosis induced by cisplatin, and, to a lesser extent, by staurosporine, as appeared after ultrastructural observations. In particular, if compared to treatments alone, samples pre-treated with melatonin before chemicals showed preserved nuclei and organelles, a reduced in situ DNA fragmentation and a decrease of lipid peroxidation events .In conclusion, these findings evidence melatonin ability in preventing mitochondrial dysfunctions and, as a consequence, the activation of skeletal muscle apoptosis.