Effect of hyperbaric oxygen and vitamin C and E supplementation on biomarkers of oxidative stress in healthy men

Insititute of Biological Chemistry and Nutrition, University of Hohenheim, Garbenstrasse 28, D-70593, Stuttgart, Germany.
British Journal Of Nutrition (Impact Factor: 3.45). 11/2007; 98(4):826-33. DOI: 10.1017/S0007114507744380
Source: PubMed


The objectives of the present study were to evaluate the effect of normobaric and hyperbaric O2 (HBO) on plasma antioxidants and biomarkers of oxidative stress in plasma and urine and to investigate the effect of a 4-week vitamin C plus E supplementation on HBO-induced oxidative stress. Nineteen healthy men were exposed to HBO (100 % O2; 240 kPa) before and after 4 weeks' supplementation with 500 mg vitamin C plus 165 mg alpha-tocopherol equivalents. Exposure to 21 % O2 at 100 kPa served as intra-individual controls (control). Samples for the analysis of plasma antioxidants and oxidative stress biomarkers were collected before and immediately after each treatment. The present results showed that when compared with 'control', a single exposure to HBO resulted in a decrease of plasma vitamin C (P = 0.027) and an increase of lipid peroxides (P = 0.0008) and urinary 8-oxo-deoxyguanosine (8-oxodG) excretion (P = 0.006). Oxidative stress was not prevented by a 4-week supplementation with vitamins C and E. HBO-induced changes in plasma parameters correlated with basal antioxidant levels. The increase of urinary 8-oxodG after HBO plus supplementation correlated negatively with vitamin E intake (P = 0.023). We concluded that in healthy men HBO caused oxidative stress, which could not be prevented by dietary vitamin C plus E supplementation. The present data support the idea that HBO is a suitable model for oxidative stress in healthy volunteers.

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    • "Previously, oxidative stress has been implicated as a key transduction signal for various cytokines and hormones (Fisher-Wellman & Bloomer, 2009; Kalmar & Greensmith, 2009). Previous data demonstrate that a single exposure to HBO results in elevated lipid peroxides (Bader et al., 2007). Although there was an increase in TBARS post-exposure following HA in the present study, however, this did not reach statistical significance (Fig. 3). "
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    ABSTRACT: Heat shock protein 72 (HSP72) is expressed in response to stress and has been demonstrated to follow a diurnal expression pattern within monocytes and is sensitive to changes in core temperature. Numerous studies have shown changes in HSP72 expression within cell lines exposed to hyperbaric conditions. No studies have investigated changes in HSP72 expression in vivo. Six males participated in the study and were exposed to hyperbaric air and hyperbaric oxygen a week apart. Monocyte HSP72 was analyzed by flow cytometry at 09:00, 13:00, 17:00, 21:00 with hyperbaric oxygen or hyperbaric air breathing commencing at 15:00 for 78 min at a pressure of 2.8 ATA. HSP72 under normoxia followed the established trend; however, following the hyperbaric air or oxygen exposure a reduction in detectable HSP72 was observed at 17:00 and 21:00. No changes in core temperature were observed between 13:00 and 21:00 for any condition. The data show that HSP72 expression is impaired following hyperbaric air (HA) exposure, when compared with control or hyperbaric oxygen (HO) exposure.
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    • "Consequently, antioxidants, such as vitamin C (VC), are widely used as therapeutic agents. However, the precise mechanism of antioxidant action is still unclear and the role of VC in oxidative stress is still controversial (Bader et al., 2007; Besaratinia et al., 2007). "
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    ABSTRACT: The aim of this study was to test the hypothesis that hepatic vitamin C (VC) levels in VC deficient mice rescued with high doses of VC supplements still do not reach the optimal levels present in wild-type mice. For this, we used a mouse scurvy model (sfx) in which the L-gulonolactone oxidase gene (Gulo) is deleted. Six age- (6 weeks old) and gender- (female) matched wild-type (WT) and sfx mice (rescued by administering 500 mg of VC/L) were used as the control (WT) and treatment (MT) groups (n = 3 for each group), respectively. Total hepatic RNA was used in triplicate microarray assays for each group. EDGE software was used to identify differentially expressed genes and transcriptomic analysis was used to assess the potential genetic regulation of Gulo gene expression. Hepatic VC concentrations in MT mice were significantly lower than in WT mice, even though there were no morphological differences between the two groups. In MT mice, 269 differentially expressed transcripts were detected (≥ twice the difference between MT and WT mice), including 107 up-regulated and 162 down-regulated genes. These differentially expressed genes included stress-related and exclusively/predominantly hepatocyte genes. Transcriptomic analysis identified a major locus on chromosome 18 that regulates Gulo expression. Since three relevant oxidative genes are located within the critical region of this locus we suspect that they are involved in the down-regulation of oxidative activity in sfx mice.
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    • "Antioxidant supplementation was used to prevent negative impacts of oxygenation therapy, however, with contradictory results. While some studies have shown protective effects of exogenously administered antioxidants [4] [5] others have failed to demonstrate prevention against oxidative damage [6]. "
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    ABSTRACT: Oxygen therapy is used for the treatment of various diseases, but prolonged exposure to high concentrations of O(2) is also associated with formation of free radicals and oxidative damage. In the present study we compared alpha-ketoglutarate dehydrogenase (KGDH) activity and mitochondrial oxidative damage in the hearts of guinea pigs after long-term (17 and 60 h) oxygenation with 100% normobaric O(2) and with partially negatively (O(2 neg)) or positively (O(2 posit)) ionized oxygen. Inhalation of O(2) led to significant loss in KGDH activity and thiol group content and accumulation of bityrosines. Inhalation of O(2 neg) was accompanied by more pronounced KGDH inhibition, possibly due to additional formation of protein-lipid conjugates. In contrast, O(2 posit) prevented loss in KGDH activity and diminished mitochondrial oxidative damage. These findings suggest that oxygen treatment is associated with impairment of heart energy metabolism and support the view that inhalation of O(2 posit) optimizes the beneficial effects of oxygen therapy.
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