Can antioxidant vitamins materially reduce oxidative damage in humans?

Citation
Mr. Mccall et B. Frei, Can antioxidant vitamins materially reduce oxidative damage in humans?, FREE RAD B, 26(7-8), 1999, pp. 1034-1053
Citations number
91
Categorie Soggetti
Biochemistry & Biophysics
Journal title
FREE RADICAL BIOLOGY AND MEDICINE
ISSN journal
08915849 → ACNP
Volume
26
Issue
7-8
Year of publication
1999
Pages
1034 - 1053
Database
ISI
SICI code
0891-5849(199904)26:7-8<1034:CAVMRO>2.0.ZU;2-4
Abstract
Endogenous oxidative damage to proteins, lipids, and DNA is thought to be a n important etiologic factor in aging and the development of chronic diseas es such as cancer, atherosclerosis, and cataract formation. The pathology a ssociated with these diseases is likely to occur only after the production of reactive oxygen species has exceeded the body's or cell's capacity to pr otect itself and effectively repair oxidative damage. Vitamin C, vitamin E, and beta-carotene, often referred to as "antioxidant vitamins," have been suggested to limit oxidative damage in humans, thereby lowering the risk of certain chronic diseases. However, epidemiological studies and clinical tr ials examining the efficacy of antioxidant vitamins, either individually or in combination, to affect disease outcome rarely address possible underlyi ng mechanisms. Thus, in these studies it is often assumed that antioxidant vitamins act by lowering oxidative damage, but evidence in support of this contention is not provided. Therefore, in this review, we examine the scien tific evidence that supplementation of humans with vitamin C, vitamin E, or p-carotene lowers in vivo oxidative damage to lipids, proteins, or DNA bas ed on the measurement of oxidative biomarkers, not disease outcome. With th e only exception of supplemental vitamin E, and possibly vitamin C, being a ble to significantly lower lipid oxidative damage in both smokers and nonsm okers, the current evidence is insufficient to conclude that antioxidant vi tamin supplementation materially reduces oxidative damage in humans. (C) 19 99 Elsevier Science Inc.