Shulin Liu1, Donald Y Shirachi2, Raymond M Quock3. 1. Department of Diving Medicine, Second Military Medical University, Shanghai, China; Department of Psychology, Washington State University, Pullman, WA 99164, USA. 2. Department of Physiology and Pharmacology, Thomas J. Long School of Pharmacy and Health Sciences, University of the Pacific, Stockton, CA 95211, USA. 3. Department of Psychology, Washington State University, Pullman, WA 99164, USA; Translational Addiction Research Center, Washington State University, Pullman, WA 99164, USA. Electronic address: quockr@wsu.edu.
Abstract
AIMS: Exposure to hyperbaric oxygen (HBO2) causes an antinociceptive response in mice. However, breathing oxygen (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. MAIN METHODS: Male NIH Swiss mice were assessed for acute antinociceptive responsiveness under room air or 100% O2 at 1.0 or 3.5 atmospheres absolute (ATA), using the acetic acid-induced abdominal constriction test. For the oxygen toxicity test, mice were exposed to 3.5 ATA oxygen for 11min, 60min, and 60min daily for 2days (120min) or 60min daily for 4days (240min), then assessed by analyzing the levels of two oxidative stress markers, MDA (malondialdehyde) and protein carbonyl in brain, spinal cord and lung. KEY FINDINGS: 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. In the oxygen toxicity test, mice exposed to HBO2 for different time intervals had levels of brain, spinal cord and lung MDA and protein carbonyl that were comparable to that of control animals exposed to room air. SIGNIFICANCE: Treatment with 100% O2 evokes a pressure-dependent antinociceptive effect. Since there was no significant increase in levels of the oxidative stress markers in the tested tissues, it is concluded that HBO2 at 3.5 ATA produces antinociception in the absence of oxidative stress in mice.
AIMS: Exposure to hyperbaric oxygen (HBO2) causes an antinociceptive response in mice. However, breathing oxygen (O2) at an elevated pressure can potentially cause oxygentoxicity. The aim of this study was to identify the determinants of HBO2 antinociception and the toxicity profile of HBO2. MAIN METHODS: Male NIH Swissmice were assessed for acute antinociceptive responsiveness under room air or 100% O2 at 1.0 or 3.5 atmospheres absolute (ATA), using the acetic acid-induced abdominal constriction test. For the oxygentoxicity test, mice were exposed to 3.5 ATA oxygen for 11min, 60min, and 60min daily for 2days (120min) or 60min daily for 4days (240min), then assessed by analyzing the levels of two oxidative stress markers, MDA (malondialdehyde) and protein carbonyl in brain, spinal cord and lung. KEY FINDINGS: 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. In the oxygentoxicity test, mice exposed to HBO2 for different time intervals had levels of brain, spinal cord and lung MDA and protein carbonyl that were comparable to that of control animals exposed to room air. SIGNIFICANCE: Treatment with 100% O2 evokes a pressure-dependent antinociceptive effect. Since there was no significant increase in levels of the oxidative stress markers in the tested tissues, it is concluded that HBO2 at 3.5 ATA produces antinociception in the absence of oxidative stress in mice.
Authors: Carlee R Gibbons; Shulin Liu; Yangmiao Zhang; Casey L Sayre; Briana R Levitch; Sarah B Moehlmann; Donald Y Shirachi; Raymond M Quock Journal: Brain Res Date: 2013-08-30 Impact factor: 3.252