Abstract
Exposure to 3.5 ATA HBO2 causes antinociception in mice (Ohgami et al., NeuroReport 20:1325, 2010). However, breathing O2 at an elevated pressure can potentially cause oxygen toxicity. The aim of this study was to identify the determinants of HBO2 antinociception and the toxicity profile of HBO2. Male NIH Swiss mice were assessed for acute antinociceptive responsiveness under room air or 100% O2 at 1.0 or 3.5 ATA, using the acetic acid‐induced abdominal constriction test. Only the combination of 100% O2 and 3.5 ATA caused significant antinociception. The antinociceptive effect of 100% O2 was pressure‐dependent up to 3.5 ATA. Oxygen toxicity was assessed by analyzing the levels of two oxidative stress markers, MDA (malondialdehyde) and protein carbonyl, in brain, spinal cord and lung after HBO2 exposure. The results showed no significant increase of either marker in the tested tissues, indicating an absence of significant oxidative stress caused by an 11‐min HBO2 treatment. In fact, even a 60‐min HBO2 treatment failed to produce any significant changes. It is concluded that HBO2 at 3.5 ATA is able to produce significant antinociception without causing oxygen toxicity in mice. (This research was supported by NIH Grant AT‐007222 and the Allen I. White Distinguished Professorship at Washington State University.)
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