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Major sources of reactive oxygen species in living systems. The mitochondrial theory of aging was first proposed in 1978, [27] [28] and two years later, the mitochondrial free-radical theory of aging was introduced. [29]
During ATP production electrons can escape the mitochondrion and react with water, producing reactive oxygen species, ROS for short. ROS can damage macromolecules, including lipids, proteins and DNA, which is thought to facilitate the process of ageing. Electron transport chain in the inner mitochondrial membrane
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 ]
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.
Specific examples include stroke and heart attack. [citation needed] In general, the harmful effects of reactive oxygen species on the cell are the damage of DNA or RNA, oxidation of polyunsaturated fatty acids in lipids (lipid peroxidation), oxidation of amino acids in proteins, and oxidative deactivation of specific enzymes by oxidation co ...
The structure of her meals is always the same: vegetables, high-quality proteins, healthy fats, and carbohydrates that don't spike her blood sugar too much, she said.
Although oxidative phosphorylation is a vital part of metabolism, it produces reactive oxygen species such as superoxide and hydrogen peroxide, which lead to propagation of free radicals, damaging cells and contributing to disease and, possibly, aging and senescence.
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