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Mechanisms and Biomarkers (WG 4) page 24
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adequate but that the protective margin is relatively small. In humans, it was shown that
dietary supplementation with vitamin E increased tissue resistance to exercise-induced lipid
peroxidation (Kanter et al., 1993). No data on specific oxidative markers were obtained with
vitamin C supplementation. GSH deficiency has been associated with decreased GSH status
and increased lipid peroxidation after exercise. GSH and N-acetyl-cysteine supplementation
may improve endurance and decrease lipid peroxidation. Finally, studies on antioxidant
enzymes clearly showed an adaptation of these latter to exercise. This is particularly true for
superoxide dismutase which has been shown to increase after an acute bout of exercise
(Lawler et al., 1993). This activation was proposed to result from increased superoxide anion
production during exercise. These relatively early studies now opened to the concept that
reactive oxygen species may have an essential role in signal transduction at the cell level :
- through a chemical recognition system involving their ability to interact and covalently
modify selected targets of protein components, thiol groups of cysteine residues or heme iron
(Lander, 1997)
- by regulation of the nuclear transcription factors sensitive to redox status of cells, including
AP-1 and NF-kB (Flohé et al., 1997).
Antioxidant status
The balance between antioxidants and prooxidants in living organism may be defined as
antioxidant status. This balance is dynamic and slightly in favour of oxidation since DNA,
lipid and protein oxidation is ongoing throughout life. The body’s antioxidant including repair
systems are adapted to this imbalance. Antioxidant status is multiparametric and depends on
genetics, physiological state but also on environment and diet. Oxidative stress thus represents
a more serious imbalance where the primary line of defence represented by the enzymatic
systems that are overwhelmed leading to the use of a secondary line of antioxidants including
vitamins, glutathione and carotenoids. Depletion of such antioxidants should raise the level of
prooxidants including reactive oxygen and nitrogen species. As a consequence, oxidative
stress ultimately leads to damage of lipids, proteins, carbohydrates and DNA bases. An
evaluation of antioxidant status may consist of determination of components belonging either
to the primary line of defence (i.e. enzymes) and/or the secondary line of defence (other
proteins and low-molecular weight compounds) and/or the oxidised biomolecules. However,
the main interest of antioxidant status determination is to link this status to pathological
conditions such as cancer or cardiovascular diseases. One main difficulty to assess such a
relationship is to identify early biomarkers which can surrogate for pathophysiological