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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 ...
Reactive oxygen species are implicated in cellular activity to a variety of inflammatory responses including cardiovascular disease. They may also be involved in hearing impairment via cochlear damage induced by elevated sound levels , in ototoxicity of drugs such as cisplatin , and in congenital deafness in both animals and humans.
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.
Mitochondrial ROS can promote cellular senescence and aging phenotypes in the skin of mice. [11] Ordinarily mitochondrial SOD2 protects against mitochondrial ROS. Epidermal cells in mutant mice with a genetic SOD2 deficiency undergo cellular senescence, nuclear DNA damage, and irreversible arrest of proliferation in a portion of their keratinocytes.
These radicals remain in ground state and react with oxygen, leading to the formation of reactive oxygen species (ROS) and superoxide anion radicals (O2•−), which further react with oxygen to generate ROS. [8] The chain of reactions that generate reactive oxygen species (ROS) results in oxidative stress, which ultimately causes cell damage ...
During the process of aging, an organism accumulates damage to its macromolecules, cells, tissues, and organs.Specifically, aging is characterized as and thought to be caused by "genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular ...
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