Calorie restriction reduces oxidative stress by SIRT3-mediated SOD2 activation.

By Xiaolei Qiu, Katharine Brown, M. Hirschey, E. Verdin, Danica Chen. Cell Metabolism, 2010

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The hallmarks of aging. (2013, background): “SIRT3 may also directly control the rate of ROS production by deacetylating manganese superoxide dismutase, a major mitochondrial antioxidant enzyme (Qiu et al., 2010; Tao et al., 2010).”
The NAD+ precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet induced obesity (2012, neutral): “, 2004) and SOD2 (Qiu et al., 2010), respectively) was observed in the skeletal muscle, liver and BAT, where NAD+ content was induced by NR, but not in brain and WAT, where NAD+ levels were unaffected by NR supplementation (Fig.”
SIRT3 Deficiency and Mitochondrial Protein Hyperacetylation Accelerate the Development of the Metabolic Syndrome (2011, neutral): “, 2008), and increased reactive oxygen species (Kim et al., 2010; Qiu et al., 2010; Someya et al., 2010; Tao et al., 2010).”
Sirtuins as regulators of metabolism and healthspan (2012, background): “More recently, it became apparent that SIRT3 also affects oxidative stress defence by protecting cells from reactive oxygen species (ROS”
SIRT3 opposes reprogramming of cancer cell metabolism through HIF1α destabilization (2011, background): “Additionally, SIRT3 can directly target IDH2, influencing cellular redox status, and SOD2, activating mitochondrial ROS scavenging (Qiu et al., 2010; Someya et al., 2010; Tao et al., 2010).”