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The free radical theory of aging states that organisms age because cells accumulate free radical damage over time. [1] A free radical is any atom or molecule that has a single unpaired electron in an outer shell. [2] While a few free radicals such as melanin are not chemically reactive, most biologically relevant free radicals are highly ...
Molecular contributors to ageing (reactive oxygen species, mitochondrial unfolded protein response, mitochondrial metabolites, damage-associated molecular patterns, mitochondrial-derived peptides, mitochondrial membrane) Mitochondria are thought to be organelles that developed from endocytosed bacteria which learned to coexist inside ancient cells.
In normal conditions, the oxygen is reduced to produce water; however, in about 0.1–2% of electrons passing through the chain (this number derives from studies in isolated mitochondria, though the exact rate in live organisms is yet to be fully agreed upon), oxygen is instead prematurely and incompletely reduced to give the superoxide radical ...
Catalase is an enzyme that removes hydrogen peroxide, a reactive oxygen species, and thus limits oxidative DNA damage. In mice, when catalase expression is increased specifically in mitochondria, oxidative DNA damage (8-OHdG) in skeletal muscle is decreased and lifespan is increased by about 20%.
Though the idea is controversial, some evidence suggests a link between aging and mitochondrial genome dysfunction. [86] In essence, mutations in mtDNA upset a careful balance of reactive oxygen species (ROS) production and enzymatic ROS scavenging (by enzymes like superoxide dismutase, catalase, glutathione peroxidase and others).
The most commonly used test is called a TBARS Assay (thiobarbituric acid reactive substances assay). Thiobarbituric acid reacts with malondialdehyde to yield a fluorescent product. However, there are other sources of malondialdehyde, so this test is not completely specific for lipid peroxidation. [14]
Reactive oxygen species levels increase with age in these mutant strains and show a similar pattern to the pattern of DNA damage increase with age. Thus it appears that superoxide dismutase plays a substantial role in preserving genome integrity during aging in S. cerevisiae. SOD2 knockout or null mutations cause growth inhibition on ...
In wild-type budding yeast Saccharomyces cerevisiae nuclear DNA fragmentation increased 3-fold during cellular aging, whereas in the absence of SOD2 nuclear DNA fragmentation increased by 5-fold during aging. [23] Production of reactive oxygen species also increased with cellular age, but by a greater amount in SOD2 mutant cells than in wild ...