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Verfasst von:Dröge, Wulf [VerfasserIn]   i
Titel:Free radicals in the physiological control of cell function
Verf.angabe:Wulf Dröge
E-Jahr:2002
Jahr:01 Jan 2002
Umfang:49 S.
Fussnoten:Gesehen am 03.02.2021
Titel Quelle:Enthalten in: Physiological reviews
Ort Quelle:Bethesda, Md. [u.a.] : Soc., 1921
Jahr Quelle:2002
Band/Heft Quelle:82(2002), 1, Seite 47-95
ISSN Quelle:1522-1210
Abstract:At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, however, nitric oxide (NO), superoxide anion, and related reactive oxygen species (ROS) play an important role as regulatory mediators in signaling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and reestablish “redox homeostasis.” Higher organisms, however, have evolved the use of NO and ROS also as signaling molecules for other physiological functions. These include regulation of vascular tone, monitoring of oxygen tension in the control of ventilation and erythropoietin production, and signal transduction from membrane receptors in various physiological processes. NO and ROS are typically generated in these cases by tightly regulated enzymes such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively. In a given signaling protein, oxidative attack induces either a loss of function, a gain of function, or a switch to a different function. Excessive amounts of ROS may arise either from excessive stimulation of NAD(P)H oxidases or from less well-regulated sources such as the mitochondrial electron-transport chain. In mitochondria, ROS are generated as undesirable side products of the oxidative energy metabolism. An excessive and/or sustained increase in ROS production has been implicated in the pathogenesis of cancer, diabetes mellitus, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia/reperfusion injury, obstructive sleep apnea, and other diseases. In addition, free radicals have been implicated in the mechanism of senescence. That the process of aging may result, at least in part, from radical-mediated oxidative damage was proposed more than 40 years ago by Harman (J Gerontol 11: 298-300, 1956). There is growing evidence that aging involves, in addition, progressive changes in free radical-mediated regulatory processes that result in altered gene expression.
DOI:doi:10.1152/physrev.00018.2001
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1152/physrev.00018.2001
 Volltext: https://journals.physiology.org/doi/full/10.1152/physrev.00018.2001
 DOI: https://doi.org/10.1152/physrev.00018.2001
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1747171026
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