Clinical biochemistry · 2005
Correlation between hyperbaric oxygen exposure pressures and oxidative parameters in rat lung, brain, and erythrocytes.
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Oter Sukru, Korkmaz Ahmet, Topal Turgut, Ozcan Omer, Sadir Serdar, Ozler Mehmet, Ogur Recai, Bilgic Hayati
Аннотация
OBJECTIVES: The oxygen toxicity risk of hyperbaric oxygen (HBO) treatment has long been of interest. However, there are no comprehensive articles describing the relationship between HBO protocols and oxidative parameters used clinically. The purpose of this study was to determine the effects of various HBO pressure modalities on the oxidative values of rat lung, brain, and erythrocytes.
DESIGN AND METHODS: A total of 64 male Sprague-Dawley rats was randomly divided into 7 groups. Group A was used as a control. Groups C to G were subjected to 100% oxygen at a pressure of 1, 1.5, 2, 2.5, and 3 ATA (atmosphere absolute), respectively, for 2 h. Group B was exposed to normal atmospheric air at 3 ATA for the same duration. The rat's lung, brain, and blood were taken immediately after the exposure and thiobarbituric acid reactive substances (TBARS) and superoxide dismutase (SOD) levels were determined.
RESULTS: Both TBARS levels and SOD activity increased concordantly with the pressure increase. Although a statistically significant change in TBARS levels started from 100% oxygen exposure at 1 ATA (normobaric), SOD activity was affected after 2 ATA. A significant correlation exists between exposure pressure and the aforementioned parameters. Ambient air exposure at 3 ATA did not affect any parameters besides the brain TBARS levels.
CONCLUSIONS: It is clear that HBO exposure causes oxidative stress. The main reason for this effect seems to be exposure to pure oxygen, since pure high pressure has no significant effect on the aforementioned parameters. However, clinicians should use as low pressures as possible since all oxidative parameters appear to be directly proportional to the extent of HBO exposure.
DESIGN AND METHODS: A total of 64 male Sprague-Dawley rats was randomly divided into 7 groups. Group A was used as a control. Groups C to G were subjected to 100% oxygen at a pressure of 1, 1.5, 2, 2.5, and 3 ATA (atmosphere absolute), respectively, for 2 h. Group B was exposed to normal atmospheric air at 3 ATA for the same duration. The rat's lung, brain, and blood were taken immediately after the exposure and thiobarbituric acid reactive substances (TBARS) and superoxide dismutase (SOD) levels were determined.
RESULTS: Both TBARS levels and SOD activity increased concordantly with the pressure increase. Although a statistically significant change in TBARS levels started from 100% oxygen exposure at 1 ATA (normobaric), SOD activity was affected after 2 ATA. A significant correlation exists between exposure pressure and the aforementioned parameters. Ambient air exposure at 3 ATA did not affect any parameters besides the brain TBARS levels.
CONCLUSIONS: It is clear that HBO exposure causes oxidative stress. The main reason for this effect seems to be exposure to pure oxygen, since pure high pressure has no significant effect on the aforementioned parameters. However, clinicians should use as low pressures as possible since all oxidative parameters appear to be directly proportional to the extent of HBO exposure.