Abstract
Updating the Free Radical Theory of Aging
Highlights
The free radical theory of aging, one of the nine suggested hallmarks of aging (López-Otín et al, 2016), implicates the gradual accumulation of oxidative cellular damage as a fundamental driver of cellular aging (Harman, 1956; Miquel et al, 1980)
These results suggest that the chronic immune activation and subsequent oxidative stress induced by human immunodeficiency virus (HIV) may lead to de novo mitochondrial DNA (mtDNA) mutations, while oxidative damage associated with exposure to tobacco smoking may promote the clonal amplification of pre-existing mtDNA mutations (Figure 1)
Mirroring the results in humans (Kennedy et al, 2013; Ziada et al, 2019), a recent study in Drosophila showed that age was associated with accumulation of somatic mtDNA transition, but not transversion, mutations suggesting that the role of polymerase γ errors in mitochondrial aging is not limited to humans (Itsara et al, 2014)
Summary
The free radical theory of aging, one of the nine suggested hallmarks of aging (López-Otín et al, 2016), implicates the gradual accumulation of oxidative cellular damage as a fundamental driver of cellular aging (Harman, 1956; Miquel et al, 1980). This theory has evolved over time to emphasize the role of free radical induced mitochondrial DNA (mtDNA) mutations and the accumulation of mtDNA deletions (Miquel et al, 1980; Cortopassi et al, 1992; Michikawa et al, 1999). The observation of oxidative damage in the form of 7,8-dihydro-8-oxo-deoxyguanosine (8-oxodG) DNA oxidative lesions accumulating with age has been a cornerstone of the free radical theory of aging (Fraga et al, 1990)
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