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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.
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.
Hyperbaric oxygen chambers contain a pure, pressurized form of the gas to increase its absorption in the body. They are used to treat conditions including burns, wounds, skin and bone infections ...
Oxidative stress mechanisms in tissue injury. Free radical toxicity induced by xenobiotics and the subsequent detoxification by cellular enzymes (termination).. Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. [1]
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.
Cells can also be induced to senesce by DNA damage in response to elevated reactive oxygen species (ROS), activation of oncogenes, and cell-cell fusion. Normally, cell senescence is reached through a combination of a variety of factors (i.e., both telomere shortening and oxidative stress). [13]
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