The Effects of Hyperbaric Oxygen at Different Pressures on Oxidative Stress and Antioxidant Status in Rats

Abstract

Background: The optimal use of oxygen at greater than atmospheric pressures in any operational or therapeutic application (hyperbaric oxygen, HBO2) requires awareness of the fact that the beneficial effects of oxygen coexist with toxic effects depending on the pressure and duration of exposure. In this study, we aimed to investigate the effect of HBO2 therapy on oxidative stress and antioxidant status in commonly used protocol for acute HBO2 indications, such as carbon monoxide intoxication, central retinal artery occlusion, crush injury, gas gangrene, and to compare it with normobaric oxygen (NBO2) in healthy rats. Materials and Methods: Fifty-six male, young adult Wistar albino rats were randomly divided into seven groups and named as Group I through Group VII. Plasma malondialdehyde (MDA), superoxide dismutase (SOD), and erythrocyte glutathione (GSH) levels in control group were compared to the levels in other groups. Results: The increases in MDA levels and the decrease in SOD activities were statistically significant in HBO2 groups at the end of the first 24 h when compared to the control group, and the significant decrease in erythrocyte GSH level was only at 2.4 atmospheres absolute. Conclusions: The present study showed that pressure and frequency of exposure are important factors to consider when investigating HBO2-induced oxidative stress and antioxidant response.

Hyperbaric Oxygen Therapy Improves the Osteogenic and Vasculogenic Properties of Mesenchymal Stem Cells in the Presence of Inflammation In Vitro

“…During HBO treatment (100% O 2 ), the PaO 2 in tissues rises to around 1500 mm Hg, which corresponds to pO 2 of 500 mm Hg in soft tissue and 200 mm Hg in bone [4]. It is well accepted that such exposure to high oxygen concentrations increases the formation of reactive oxygen species (ROS), which in turn results in consumption of antioxidants and reduction of antioxidant enzyme activity [40]. Furthermore, ROS can react with macromolecular components, inducing cells necrosis or apoptosis [41].…”

Use of hyperbaric oxygen therapy for preventing delayed neurological sequelae in patients with carbon monoxide poisoning: A multicenter, prospective, observational study in Japan

“…HBO 2 reduced oxidative stress in an animal model of CO poisoning [26] and its beneficial effects included inhibition of leukocyte beta-2 integrins [18], reversal of CO-cytochrome c oxidase binding [27], and recovery of energy metabolism [28]. However, there have been reports that HBO 2 therapy itself induces oxidative stress [29][30][31][32]. Experimental data have shown that HBO 2 induces oxidative stress in healthy rat brains, measured as the lipid peroxidation products in brain cortex homogenates [29][30][31].…”

“…However, there have been reports that HBO 2 therapy itself induces oxidative stress [29][30][31][32]. Experimental data have shown that HBO 2 induces oxidative stress in healthy rat brains, measured as the lipid peroxidation products in brain cortex homogenates [29][30][31]. This HBO 2 -induced oxidative stress is related to the HBO 2 pressure [29] or the exposure time [30].…”

Hyperbaric oxygen treatment impacts oxidative stress markers in patients with necrotizing soft-tissue infection

“…20 21 Moreover, HBO 2 -mediated alterations of the two antioxidants, heme oxygenase-1 (HO-1) and superoxide dismutase (SOD), have been demonstrated in experimental models of sepsis associated acute lung injury, in sepsis, and as part of a protective mechanism against oxidative DNA damage. [22][23][24][25][26][27] Multiple HBO 2 treatments have been shown to elevate RNS by enhancing production of nitrite+nitrate in selected cohorts, 28 but the systemic effect on RNS remains unresolved. 29 30 Of notable interest is a SODmediated regulatory function of NO expression 31 and an inhibitory function of HO-1 on the NO synthase expression, 32 indicating closely interconnected regulatory mechanisms between RNS and ROS.…”