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Hyperoxia exposure alters hepatic eicosanoid metabolism in newborn mice
Lynette K Rogers1, Trent E Tipple, Rodney D Britt
1Center for Perinatal Research, Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, Ohio State University, 700 Children's Dr., Columbus, Ohio 43205, USA. Lynette.Rogers@NationwideChildrens.org
Insights
Newborn mice exposed to high oxygen levels experienced lung injury and liver metabolic changes. This research explores early responses in neonatal hyperoxic lung injury, potentially revealing new therapeutic targets for bronchopulmonary dysplasia.
Area of Science:
- Neonatal physiology
- Pulmonary medicine
- Toxicology
Background:
- Premature infants often receive high oxygen concentrations, risking lung injury and bronchopulmonary dysplasia.
- The lung-liver relationship during hyperoxic lung injury is poorly understood in neonates.
- This study investigates oxidant stress in neonatal livers due to hyperoxia.
Purpose of the Study:
- To test the hypothesis that oxidant stress occurs in the livers of newborn mice exposed to continuous hyperoxia.
- To explore the relationship between lung and liver responses to hyperoxia in neonates.
- To identify potential mechanisms of hyperoxic lung injury in a neonatal model.
Main Methods:
- Exposure of newborn mice to continuous hyperoxia versus room air.
- Measurement of oxidative stress markers (glutathione disulfide, nitrotyrosine) in lung and liver tissues.
- Analysis of lipid metabolism markers (5-lipoxygenase, cyclooxygenases-2, hydroxyeicosatetraenoic acid, prostaglandin) in liver tissues.
Main Results:
- Increased glutathione disulfide and nitrotyrosine in lung tissues, but not liver tissues, of hyperoxia-exposed mice.
- Early increases in 5-lipoxygenase and cyclooxygenases-2 protein levels in the liver tissues of hyperoxia-exposed pups.
- Elevated levels of hydroxyeicosatetraenoic acid and prostaglandins in the liver tissues of hyperoxia-exposed pups.
Conclusions:
- Free radical oxidation is confirmed in the lungs of newborn mice exposed to hyperoxia.
- Alterations in lipid metabolism in liver tissues may represent a primary response to hyperoxia in neonates.
- Findings suggest novel mechanisms in neonatal bronchopulmonary dysplasia, opening avenues for future research.
Abstract:
Prematurely born infants are often treated with supraphysiologic amounts of oxygen, which is associated with lung injury and the development of diseases such as bronchopulmonary dysplasia. Complimentary responses between the lung and liver during the course of hyperoxic lung injury have been studied in adult animals, but little is known about this relationship in neonates. These studies tested the hypothesis that oxidant stress occurs in the livers of newborn mice in response to continuous hyperoxia exposure. Greater levels of glutathione disulfide and nitrotyrosine were detected in lung tissues but not liver tissues from newborn mice exposed to hyperoxia than in room air-exposed controls. However, early increases in 5-lipoxygenase and cyclooxygenases-2 protein levels and increases in total hydroxyeicosatetraenoic acid and prostaglandin levels were observed in the liver tissues of hyperoxia-exposed pups. These studies indicate that free radical oxidation occurs in the lungs of newborn pups exposed to hyperoxia, and alterations in lipid metabolism could be a primary response in the liver tissues. The findings of this study identify possible new mechanisms associated with hyperoxic lung injury in a newborn model of bronchopulmonary dysplasia and thus open opportunities for research.
