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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. Disturbances in the normal redox state of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA. Oxidative stress from oxidative metabolism causes base damage, as well as strand breaks in DNA. Base damage is mostly indirect and caused by reactive oxygen species (ROS) generated, e.g. O2− (superoxide radical), OH (hydroxyl radical) and H2O2 (hydrogen peroxide).〔Kala Chandra, Ali Syed Salman *, Abid Mohd., Rajpoot Sweety, Khan Najam Ali. Protection Against FCA Induced Oxidative Stress Induced DNA Damage as a Model of Arthritis and In vitro Anti-arthritic Potential of Costus speciosus Rhizome Extract. (www.ijppr.com ) International Journal of Pharmacognosy and Phytochemical Research 2015; 7(2); 383-389. ISSN: 0975-4873〕 Further, some reactive oxidative species act as cellular messengers in redox signaling. Thus, oxidative stress can cause disruptions in normal mechanisms of cellular signaling. In humans, oxidative stress is thought to be involved in the development of Asperger syndrome, ADHD, cancer,〔 Parkinson's disease, Lafora disease, Alzheimer's disease, atherosclerosis, heart failure, myocardial infarction, fragile X syndrome, Sickle Cell Disease, lichen planus, vitiligo, autism, infection, and chronic fatigue syndrome. However, reactive oxygen species can be beneficial, as they are used by the immune system as a way to attack and kill pathogens. Short-term oxidative stress may also be important in prevention of aging by induction of a process named mitohormesis. ==Chemical and biological effects== Chemically, oxidative stress is associated with increased production of oxidizing species or a significant decrease in the effectiveness of antioxidant defenses, such as glutathione. The effects of oxidative stress depend upon the size of these changes, with a cell being able to overcome small perturbations and regain its original state. However, more severe oxidative stress can cause cell death and even moderate oxidation can trigger apoptosis, while more intense stresses may cause necrosis. Production of reactive oxygen species is a particularly destructive aspect of oxidative * stress. Such species include free radicals and peroxides. Some of the less reactive of these species (such as superoxide) can be converted by oxidoreduction reactions with transition metals or other redox cycling compounds (including quinones) into more aggressive radical species that can cause extensive cellular damage. Most long-term effects are caused by damage to DNA. DNA damage induced by ionizing radiation is similar to oxidative stress, and these lesions have been implicated in aging and cancer. Biological effects of single-base damage by radiation or oxidation, such as 8-oxoguanine and thymine glycol, have been extensively studied. Recently the focus has shifted to some of the more complex lesions. Tandem DNA lesions are formed at substantial frequency by ionizing radiation and metal-catalyzed H2O2 reactions. Under anoxic conditions, the predominant double-base lesion is a species in which C8 of guanine is linked to the 5-methyl group of an adjacent 3'-thymine (G(Me )T). Most of these oxygen-derived species are produced at a low level by normal aerobic metabolism. Normal cellular defense mechanisms destroy most of these. Likewise, any damage to cells is constantly repaired. However, under the severe levels of oxidative stress that cause necrosis, the damage causes ATP depletion, preventing controlled apoptotic death and causing the cell to simply fall apart. Polyunsaturated fatty acids, particularly arachidonic acid and linoleic acid, are primary targets for free radical and singlet oxygen oxidations. For example, in tissues and cells, the free radical oxidation of linoleic acid produces racemic mixtures of 13-hydroxy-9''Z'',11''E''-octadecadienoic acid, 13-hydroxy-9''E'',11''E''-octadecadienoic acid, 9-hydroxy-10''E'',12-''E''-octadecadienoic acid (9-EE-HODE), and 11-hydroxy-9''Z'',12-''Z''-octadecadienoic acid as well as 4-Hydroxynonenal while singlet oxygen attacks linoleic acid to produce (presumed but not yet proven to be racemic mixtures of) 13-hydroxy-9''Z'',11''E''-octadecadienoic acid, 9-hydroxy-10''E'',12-''Z''-octadecadienoic acid, 10-hydroxy-8''E'',12''Z''-octadecadienoic acid, and 12-hydroxy-9''Z''-13-''E''-octadecadienoic (see 13-Hydroxyoctadecadienoic acid and 9-Hydroxyoctadecadienoic acid).〔〔J Oleo Sci. 2015;64(4):347-56. doi: 10.5650/jos.ess14281〕 Similar attacks on arachidonic acid produce a far larger set of products including various isoprostanes, hydroperoxy- and hydroxy- eicosatetraenoates, and 4-hydroxyalkenals.〔 While many of these products are used as markers of oxidative stress, the products derived from linoleic acid appear far more predominant than arachidonic acid products and therefore easier to identify and quantify in, for example, atheromatous plaques.〔Atherosclerosis. 2003 Mar;167(1):111-20〕 Certain of he linoleic acid products have also been proposed to be markers for specific types of oxidative stress. For example, the presence of racemic 9-HODE and 9-EE-HODE mixtures reflects free radical oxidation of linoleic acid whereas the presence of racemic 10-hydroxy-8''E'',12''Z''-octadecadienoic acid and 12-hydroxy-9''Z''-13-''E''-octadecadienoic acid reflects singlet oxygen attack on linoleic acid.〔〔Free Radic Biol Med. 2015 Feb;79:164-75. doi: 10.1016/j.freeradbiomed.2014.12.004〕 In addition to serving as markers, the linoleic and arachidonic acid products can contribute to tissue and/or DNA damage but also act as signals to stimulate pathways which function to combat oxidative stress. Table adapted from. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Oxidative stress」の詳細全文を読む スポンサード リンク
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