Oxidative stress, antioxidant defenses and nitric oxide production following hyperoxic exposures
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2013-04-01
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Little data exist on the dose-response relationship between the partial pressure of inspired oxygen (PiO2) and the cellular oxidative stress response in humans. The objective of this study was to determine the effects of PiO2 on lipid peroxidation, antioxidant enzyme activity and nitric oxide (NO) production. Twelve healthy male divers breathed 100% O2 in a hyperbaric chamber for two hours at 1 (101 kPa), 1.5 (152 kPa) and 2 (203 kPa) atmospheres absolute (atm abs). Venous blood was collected pre-, within 15 minutes post-, one and two hours post-hyperoxic exposures to determine changes in plasma and erythrocyte lipid peroxidation (thiobarbituric acid reactive substances-TBARS), antioxidant enzyme activity (superoxide dismutase-SOD), catalase-CAT, glutathione peroxidase-GPx), and plasma NO production (L-arginine [L-Arg], asymmetric dimethylarginine-ADMA, and nitrites). There were minor changes in TBARS and mixed responses in plasma and erythrocyte CAT and GPx activity. Plasma L-Arg increased following 1 and 1.5 atm abs exposures, yet ADMA and nitrites were unchanged. Only erythrocyte CAT and plasma GPx activity, and plasma L-Arg/ADMA demonstrated a significant PiO2 dose-dependent relationship. Two-hour hyperoxic exposures at 1-2 atm abs of O2 results in mixed oxidant-antioxidant responses and unaltered NO production. Moreover, there does not appear to be a strong systemic dose-dependent oxidative stress response at these hyperoxic exposures
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Scholars@Duke
Heath Gasier
I am a physiologist who joined Duke University in 2019 after retiring from military service. My research has focused on understanding how oxidant stress impacts cellular and systems physiology. Initially, I studied in humans how hyperbaric oxygen (HBO2) within the therapeutic range and high altitude influence nitric oxide production, antioxidant defenses, tissue oxygenation and muscle performance. This work sparked my interest in redox biology and led me to train under Dr. Claude A. Piantadosi at Duke University. Here, I began to study in mice and rats the impact of extreme HBO2 on the central nervous system (CNS). The objectives were to identify in rodents the origin and mechanisms of CNS oxygen toxicity, and test targeted pharmacological intervention strategies. It was during this time that I became interested in heme oxygenase 1 (HO-1). During my final military assignment, I continued to work on HBO2 and CNS oxygen toxicity related research (pharmacological intervention) and initiated new studies examining how HO-1 induction influences musculoskeletal health in diet-induced obesity. These studies led to follow-on work aimed at determining the mechanisms of HO-1 induction and mitochondrial dynamic regulation in an in vitro model of diet-induced obesity. In addition, I was involved in research aimed at understanding how antioxidants influence skeletal muscle mitochondrial dynamics in rodents and cells exposed heat stress and extreme high altitude.
Since returning to Duke University, I continue to conduct research focused on understanding how oxidant stress induced by HBO2 and obesity influences mitochondrial dynamic regulation in the brain, lung and skeletal muscle. I am now studying how sarcopenia and gender influence these responses. I am also involved (Co-I) in research testing the efficacy of a home-based high intensity interval training program in COVID-19 critical illness and early parenteral nutrition in abdominal trauma victims. In both of these studies, my efforts will be directed towards measuring inflammation and mitochondrial quality control responses to the interventions, which are linked to HO-1 activation.
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