The idea that free radicals, and in particular reactive oxygen species (ROS) produced from normal metabolism could be the primary cause of aging was proposed by Harman in the early 1950s. Years after proposing the Free Radical Theory of Aging, Harman updated this theory with the “mitochondrial theory of aging” (Lee and Wei 2012, Bereiter-Hahn 2014), proposing that mitochondria accumulates oxidative damage caused by ROS toxicity as the organism ages. The reactive oxygen species produced from metabolic respiration are associated with detrimental effects on mitochondrial function. Mitochondrial dysfunction then leads to abnormal amounts of ROS production, which further propagates oxidative damage. Mitochondria are an intracellular organelle essential for
…show more content…
2014, LaRocca, Hearon et al. 2014). Mitochondrial dysfunction can lead to severe damage in an organism. Several mitochondrial disorders present with neurological and muscular symptoms in the afflicted. In human patients with mutations in mtDNA or in nuclear genes coding for proteins in the mitochondrial ETC show multisystem disorders that include myopathy, stroke, and hearing loss (Liu and Rando 2011). A vast majority of research on why mitochondrial dysfunction gradually develops with time has focused on mtDNA integrity. Mutations and deletions in mtDNA increase with age, and areas of aged tissue that show mitochondrial ETC dysfunction contain abundant mtDNA damage (Xie, Lu et al. 2014). These findings and many earlier studies led to the concept that continuous accumulation of mtDNA damage may cause a role in the aging
2014, LaRocca, Hearon et al. 2014). Mitochondrial dysfunction can lead to severe damage in an organism. Several mitochondrial disorders present with neurological and muscular symptoms in the afflicted. In human patients with mutations in mtDNA or in nuclear genes coding for proteins in the mitochondrial ETC show multisystem disorders that include myopathy, stroke, and hearing loss (Liu and Rando 2011). A vast majority of research on why mitochondrial dysfunction gradually develops with time has focused on mtDNA integrity. Mutations and deletions in mtDNA increase with age, and areas of aged tissue that show mitochondrial ETC dysfunction contain abundant mtDNA damage (Xie, Lu et al. 2014). These findings and many earlier studies led to the concept that continuous accumulation of mtDNA damage may cause a role in the aging