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Linus Pauling Institute, Oregon State University, Corvallis, Oregon 97331-6512, USA
1Correspondence: Conference Co-chair and Co-editor, Molecular and Biological Mechanisms of Antioxidant Action, and Director, Linus Pauling Institute, Oregon State University, 571 Weniger Hall, Corvallis, OR 97331-6512, USA. E-mail Balz.Frei{at}orst.edu
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INTRODUCTION |
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The antioxidant enzymes are complemented by small-molecule
antioxidants, some of which are derived exclusively from the diet and
are vitamins. These small-molecule antioxidants are present extra- and
intracellularly, and include ascorbic acid (vitamin C), glutathione
(GSH), and tocopherols (primarily 
-tocopherol; vitamin E).
Intracellular concentrations of these compounds can be substantial,
i.e., in the millimolar range both for ascorbate and GSH.
-Tocopherol is by far the most abundant lipid-soluble antioxidant in
humans, present in cellular and subcellular membranes and lipoproteins.
The mechanisms by which these antioxidants act at the molecular and
cellular level include roles in gene expression and regulation,
apoptosis, and signal transduction. Thus, antioxidants are involved in
fundamental metabolic and homeostatic processes. However, there are
still many gaps in our knowledge of the basic mechanisms of oxidative
damage and antioxidant defenses. Filling these gaps would allow us to
more specifically target treatments and derive optimal benefits from
antioxidants for health promotion and disease prevention.
Therefore, in August of 1998, 37 national and international experts in free radical and antioxidant (bio)chemistry and cell biology met in Copper Mountain, Colo., to present their latest findings to ~150 participants at a FASEB summer research conference entitled "Molecular and Biological Mechanisms of Antioxidant Action." This conference presented a contemporary view of the mechanisms of oxidative damage to lipids, proteins, and DNA and the molecular, biochemical, and physiological action of antioxidants and their role in cell biology, with a focus on small molecule antioxidants. The sessions covered the following topics: molecular mechanisms of oxidative damage; vitamin C, vitamin E, and GSH: metabolism, antioxidant (inter)actions, and pro-oxidant vs. antioxidant effects; novel aspects of vitamin E metabolism and action; nitric oxide and radical-mediated toxicity; and (anti)oxidant regulation of gene expression: transcription factors, nuclear response elements, and apoptotic cell death.
This and the July issue of The FASEB Journal contain several
articles selected from each of these sessions and written by the
speakers. The purpose of these reviews is to provide in-depth coverage
of each topic, with emphasis on the most groundbreaking developments.
Thus, in this issue, Keaney et al. (1)
discuss the role of vitamin E as
a protein kinase C inhibitor in improving the biological activity of
endothelium-derived nitric oxide and limiting platelet aggregation and
monocyte adhesion; Stocker's group (2)
explains the novel concept of
tocopherol-mediated lipid peroxidation in lipoproteins and the
conditions under which -tocopherol acts as an antioxidant or a
pro-oxidant; May (3)
discusses the mechanisms of cellular ascorbate
recycling and a transmembrane, ascorbate-dependent oxidoreductase
activity; and Carr and I (4)
review the mechanisms by which vitamin C
may act as a pro-oxidant and the evidence in support of or against
a role of vitamin C in causing oxidative damage to biomolecules under
physiological conditions. In the July issue of the journal, articles
will address the current concepts and controversies of hepatic GSH
synthesis; provide new insights into the metabolism and function of
vitamin E; focus on the mechanisms of oxidative damage to biomolecules,
including lipid peroxidation and isolevuglandin formation, protein
oxidation and its role in atherogenic low density lipoprotein
modification, and the intriguing link between nitric oxide and the
cyclooxygenases; and, finally, discuss the role of oxidants and
antioxidants in signaling mechanisms in apoptosis and activation of the
transcription factor nuclear factor 
B.
I thank FASEB for supporting the conference and the journal for the invitation to edit this exciting series. I am grateful to my co-chair, Maret Traber, from the Linus Pauling Institute, the vice chairs Lester Packer and Steven Tannenbaum, to all who participated as speakers at the conference, and the authors and reviewers of the articles. Without the excellent contributions of these scientists, the conference and the proceedings would not have been possible.
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  M. Koyuturk, R. Yanardag, S. Bolkent, and S. Tunali The potential role of combined anti-oxidants against cadmium toxicity on liver of rats Toxicology and Industrial Health, August 1, 2007; 23(7): 393 - 401. [Abstract] [PDF]
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 K. E Hill, T. J Montine, A. K Motley, X. Li, J. M May, and R. F Burk Combined deficiency of vitamins E and C causes paralysis and death in guinea pigs Am. J. Clinical Nutrition, June 1, 2003; 77(6): 1484 - 1488. [Abstract] [Full Text] [PDF]
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