BACKGROUND/AIMS: Deleterious effects of saturated fatty acids in skeletal muscle cells are well known but their impact on mitochondrial respiration has not been well studied. Mitochondrial oxidative damage has been implicated to play a role in their effect. The purpose of this study was to evaluate viability, mtDNA integrity and mitochondrial respiration in C2C12 myoblasts and myotubes exposed to palmitate and to test the effect of mitochondria-targeted antioxidants MitoQ and MitoTEMPOL in preventing palmitate-induced damage. METHODS: Cells were treated with tested compounds, mtDNA damage was detected by quantitative PCR and mitochondrial respiration was measured using an extracellular flux analyzer XF24. RESULTS: Palmitate caused mtDNA damage, which was associated with reduced mitochondrial respiration and cell death in myoblasts but not in myotubes. MitoTEMPOL was able to prevent palmitate-induced mtDNA damage in myoblasts but failed to prevent cell death. MitoQ did not show any protective effect and both compounds markedly inhibited mitochondrial respiration. CONCLUSION: Our results indicate that skeletal muscle progenitor cells could be the first target of the deleterious action of palmitate, as myoblasts appeared to be more sensitive to its effects than myotubes possibly in part due to a lower spare respiratory capacity in the former. Only MitoTEMPOL prevented palmitate-induced mtDNA damage but neither antioxidant was able to prevent cell death and both antioxidants had a marked negative effect on respiration.

• MeSH
• Antioxidants metabolism   MeSH
• Cell Death drug effects   MeSH
• Cells, Cultured MeSH
• DNA, Mitochondrial drug effects   metabolism   MeSH
• Mitochondria drug effects   metabolism   pathology   MeSH
• Myoblasts drug effects   pathology   MeSH
• Mice MeSH
• Palmitates pharmacology   MeSH
• DNA Damage MeSH
• Animals MeSH
• Check Tag
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH

• MeSH
• Iron Chelating Agents administration & dosage   pharmacology   chemistry   MeSH
• Research Support as Topic MeSH
• Cardiovascular Diseases physiopathology   prevention & control   MeSH
• Myoblasts pathology   drug effects   MeSH
• Oxidative Stress MeSH
• Hydrogen Peroxide administration & dosage   adverse effects   MeSH
• Publication type
• Congress MeSH