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Physiological Reviews, Vol. 82, No. 1, January 2002, pp. 47-95; 10.1152/physrev.00018.2001.
Copyright ©2002 by the American Physiological Society
Division of Immunochemistry, Deutsches Krebsforschungszentrum, Heidelberg, Germany
Dröge, Wulf
Free Radicals in the Physiological Control of Cell
Function. Physiol. Rev. 82: 47-95, 2002.
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.
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