As the formation of ROS is inevitable in oxygen-consuming organisms, cells have evolved numerous mechanisms to decrease to level of oxidative stress. Therefore, a number of enzymes have strong antioxidative properties. Superoxide dismutase (SOD) for instance catalyses the dismutation reaction of the superoxide radical, which results in the production of hydrogen peroxide2,51 (H2O2). H2O2 is then in part catalytically converted into water and molecular oxygen by the enzyme catalase2, 52. The remaining part is removed by the glutathione peroxidase (GPx) which catalyses the reaction of of two molecules of reduced glutathione (GSH) and H2O2 to the oxidized form GSSG and two molecules H2O2 10, 53.
Next to to enzymatic antioxidants some vitamins have an important antioxidative effect, e.g vitamin E and C52, 53, 54. Vitamin E is located in lipoproteins and membranes where it interrupts the radical-induced chain reaction of lipidperoxidation. Vitamin C has a double function. First, it is needed to restore Vitamin E, which is transferred from alpha-tocopherol during the above-mentioned reaction to the tocopherol radical, and second, it has radical savaging properties as well. Exogenous antioxidants were also investigated with respect to their ability to blunt or even to completely prevent the oxidative damage to the DNA as described above, and at least with respect to clinical HBO therapy the question still remains unsettled whether antioxidant supplementation allows to prevent HBO-induced geno-toxicity: both vitamin E and the synthetic antioxidant N-acetylcysteine failed to affect the HBO-induced DNA damage in healthy volunteers55, but no data are available in patients with decreased antioxidant capacity. In fact, N-acetylcysteine attenuated the rise of blood lipidperoxidation markers in patients undergoing repetitive HBO treatment sessions20. Interestingly enough, in a prospective, double-blind randomised placebo-controlled study in healthy volunteers our group could recently demonstrate that a new orally effective nutritional formula (Glisodin®) containing a plant (Cucumis melo L.C) superoxide dismutase extract chemically combined with a wheat gliadin biopolymer effectively protected white-blood cell DNA from peroxidation, which coincided with reduced blood isoprostane levels56. These findings were confirmed in a subsequent in vitro study exposing isolated porcine lymphocytes to HBO-exposure resulting in a more pronounced oxidative stress than usually present during clinical HBO therapy. These findings suggest that long-term prophylactic antioxidant supplementation may indeed help to attenuate HBO-induced DNA damage.
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