Aging: Is oxidative stress a marker or is it causal?

Authors
Citation
Nk. Fukagawa, Aging: Is oxidative stress a marker or is it causal?, P SOC EXP M, 222(3), 1999, pp. 293-298
Citations number
77
Categorie Soggetti
Medical Research General Topics
Journal title
PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE
ISSN journal
00379727 → ACNP
Volume
222
Issue
3
Year of publication
1999
Pages
293 - 298
Database
ISI
SICI code
0037-9727(199912)222:3<293:AIOSAM>2.0.ZU;2-M
Abstract
Rapid developments in free radical biology and molecular technology have pe rmitted exploration of the free radical theory of aging. Oxidative stress h as also been implicated in the pathogenesis of a number of diseases. Studie s have found evidence of oxidative damage to macromolecules (DNA, lipids, p rotein), and data in transgenic Drosophila melanogaster support the hypothe sis that oxidative injury might directly cause the aging process. Additiona l links between oxidative stress and aging focus on mitochondria, leading t o development of the mitochondrial theory of aging. However, despite the nu mber of studies describing the association of markers of oxidative damage w ith advancing age, few, if any definitively link oxidative injury to altere d energy production or cellular function. Although a causal role for oxidat ive stress in the aging process has not been clearly established, this does not preclude attempts to reduce oxidative injury as a means to reduce morb idity and perhaps increase the healthy, useful life span of an individual. This review highlights studies demonstrating enhanced oxidative stress with advancing age and stresses the importance of the balance between oxidants as mediators of disease and important components of signal transduction pat hways.