Abstract
Melatonin has a wide range of physiological functions including protection against oxidative stress, which is carried out through its ability to act as a free radical scavenger and to stimulate antioxidant enzyme production (Allegra et al., 2003). Oxidative stress is a major player in initiating apoptosis in skeletal muscle, as well as in other tissues. Apoptosis is essential for skeletal muscle development and homeostasis; nevertheless, its misregulation has been frequently observed in various myopathies (Loro et al., 2010). Several authors demonstrated that melatonin exerts antiapoptotic actions in various cell models (Hibaoui et al., 2009) and our previous studies evidenced that it prevents apoptosis induced by UV-B and H2O2 in U937 cells (Luchetti et al., 2006; Salucci et al., 2010). In this work, melatonin activity has been investigated in C2C12 cells, after apoptotic chemical treatments. Myoblasts and myotubes were pre-treated with melatonin and then exposed to H2O2, cisplatin, etoposide and staurosporine. Data, obtained by means of TEM and TUNEL-CLSM, show that melatonin prevents apoptosis induced by H2O2, cisplatin and etoposide. Differently, staurosporine-induced apoptosis is not inhibited, probably because this trigger has a mechanism of action different from free radical increase. These results confirm melatonin ability to act as an antioxidant and anti-apoptotic molecule, thus suggesting a possible therapeutic strategy for myophaties involving apoptosis misregulation.
