Table 1.

Detrimental effects of ROS in skeletal muscle.

Process	Mechanism	Effect	References
Aging myocytes	Oxidation of mtDNA	Reduced capability of mitochondria to produce cellular energy	Picard et al., 2014
	mPTP opening	Mitochondrial swelling Escape of proapoptotic proteins Apoptotic or necrotic cell death	Lemasters et al., 2009; Barbieri and Sestili, 2012
	AIF and Endo G release	DNA fragmentation	Barbieri and Sestili, 2012
	Induced activity of proteases and nucleases	Apoptosis	Cadenas and Davies, 2000
Skeletal muscle contraction	Activation of calpains and caspases	Myofibrillar protein degradation	Ochala et al., 2011
	Nitrosylation of RyR1 receptor	Increase the leakiness of sarcoplasmic reticulum Ca2+	Bellinger et al., 2009; Westerblad and Allen, 2011
	Oxidation of sarcolemmal lipids or contractile proteins	Muscle dysfunction	Goldstein and Mcnally, 2010
Neuromuscular function	SOD1 deficiency	Motor axon degeneration	Fischer et al., 2011, 2012
Chronic muscle disuse	Decreased mitochondrial content; increased ROS production and apoptosis signaling	Muscle atrophy and weakness	Adhihetty et al., 2007

AIF, apoptosis inducing factor; Endo G, mitochondrial endonuclease G; mPTP, mitochondrial permeability transition pore; mtDNA, mitochondrial DNA; SOD1, Cu, Zn-superoxide dismutase.