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Creatine supplementation prevents the inhibition of myogenic differentiation in oxidatively injured C2C12 murine myoblasts
Author(s) -
Sestili Piero,
Barbieri Elena,
Martinelli Chiara,
Battistelli Michela,
Guescini Michele,
Vallorani Luciana,
Casadei Lucia,
D'Emilio Alessandra,
Falcieri Elisabetta,
Piccoli Giovanni,
Agostini Deborah,
Annibalini Giosuè,
Paolillo Marco,
Gioacchini Anna Maria,
Stocchi Vilberto
Publication year - 2009
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200800504
Subject(s) - c2c12 , myogenesis , oxidative stress , myocyte , trolox , antioxidant , creatine , microbiology and biotechnology , chemistry , oxidative phosphorylation , viability assay , biochemistry , biology , medicine , cell , antioxidant capacity
Creatine (Cr), one of the most popular nutritional supplements among athletes, has been recently shown to prevent the cytotoxicity caused by different oxidative stressors in various mammalian cell lines, including C2C12 myoblasts, via a direct antioxidant activity. Here, the effect of Cr on the differentiating capacity of C2C12 cells exposed to H 2 O 2 has been investigated. Differentiation into myotubes was monitored using morphological, ultrastructural, and molecular techniques. Treatment with H 2 O 2 (1 h) not only caused a significant (30%) loss of cell viability, but also abrogated the myogenic ability of surviving C2C12. Cr‐supplementation (24 h prior to H 2 O 2 treatment) was found to prevent these effects. Interestingly, H 2 O 2 ‐challenged cells preconditioned with the established antioxidants trolox or N ‐acetyl‐cysteine, although cytoprotected, did not display the same differentiating ability characterizing oxidatively‐injured, Cr‐supplemented cells. Besides acting as an antioxidant, Cr increased the level of muscle regulatory factors and IGF1 (an effect partly refractory to oxidative stress), the cellular availability of phosphocreatine and seemed to exert some mitochondrially‐targeted protective activity. It is concluded that Cr preserves the myogenic ability of oxidatively injured C2C12 via a pleiotropic mechanism involving not only its antioxidant capacity, but also the contribution to cell energy charge and effects at the transcriptional level which common bona fide antioxidants lack.