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Melatonin prevents mitochondrial dysfunctions and death in differentiated skeletal muscle cells
Author(s) -
Salucci Sara,
Battistelli Michela,
Baldassarri Valentina,
Burini Debora,
Falcieri Elisabetta,
Burattini Sabrina
Publication year - 2017
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/jemt.22914
Subject(s) - melatonin , myogenesis , skeletal muscle , microbiology and biotechnology , oxidative stress , apoptosis , programmed cell death , mitochondrion , myocyte , biology , dna damage , c2c12 , sarcopenia , chemistry , endocrinology , biochemistry , dna
Oxidative stress increase induces cellular damage and apoptosis activation, a mechanism believed to represent a final common pathway correlated to sarcopenia and many skeletal muscle disorders. The goal of this study is to evaluate if melatonin, a ROS scavenger molecule, is able to counteract or modulate myotube death. Here, differentiated C2C12 skeletal muscle cells have been treated with melatonin before chemicals known to induce apoptotic death and oxidative stress, and its effect has been investigated by means of morpho‐functional analyses. Ultrastructural observations show melatonin protection against triggers by the reducing of membrane blebbing, chromatin condensation, myonuclei loss and in situ DNA cleavage. Moreover, melatonin is able to prevent mitochondrial dysfunctions which occur in myotubes exposed to the trigger alone. These findings demonstrate melatonin ability in preventing apoptotic cell death in skeletal muscle fibers in vitro, suggesting for this molecule a potential therapeutic role in the treatment of various muscle disorders.