Time course and quantitative analysis of the adaptive responses to 85% oxygen in the rat lung and heart

• Published in: Biochimica et biophysica acta Vol. 1523; no. 2-3; pp. 209 - 216
• Main Authors: Evelson, Pablo, González-Flecha, Beatriz
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 18.10.2000
• Subjects: Aconitate Hydratase - metabolism; Animals; Antioxidant; Edema; Enzyme Induction; Heart - drug effects; Heart - physiology; Hyperoxia; Kinetics; Liver - drug effects; Liver - physiology; Luminescent Measurements; Lung - drug effects; Lung - physiology; Male; Oxidative Stress; Oxygen - toxicity; Rats; Rats, Sprague-Dawley; Reactive oxygen species; Superoxide Dismutase - biosynthesis; Superoxides - metabolism; Thiobarbituric Acid Reactive Substances - analysis; Time Factors; Oxidative stress; Reactive oxygen species; Antioxidant; Hyperoxia
• ISSN: 0304-4165; 0006-3002; 1872-8006
• DOI: 10.1016/S0304-4165(00)00124-0

The phenomenon of oxygen tolerance (resistance to 100% O2 in rats previously exposed to 85% O2) constitutes one of the few models of adaptive responses to oxidative stress in mammals. In vitro studies suggest that reactive oxygen species mediate this response. To test this hypothesis in vivo, we followed the time course of oxidative stress, enzyme induction, and edema in the lung, heart and liver of rats exposed to 85% O2 for 1 to 5 days. Interestingly, not only the lung, but also the heart of rats exposed to 85% O2 showed increases in the production of O⋅−2 (aconitase inactivation) early during the exposure. Increases in O⋅−2 were associated to oxidative stress (increased in situ chemiluminescence) and transient edema in both tissues. Both the lung and heart displayed induction of superoxide dismutase and reversion of the oxidative stress and damage. The adaptive response in the heart was faster and more efficient, suggesting that this tissue is at a more critical risk when exposed to elevated O2 concentrations.