Hypoxic stress exacerbates hyperoxia-induced lung injury in a neonatal mouse model of bronchopulmonary dysplasia. Academic Article uri icon

Overview

MeSH

  • Animals
  • Disease Models, Animal
  • Female
  • Glutathione
  • Humans
  • Infant, Newborn
  • Lung
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Oxidative Stress
  • Oxygen
  • Protein Carbonylation
  • Pulmonary Alveoli

MeSH Major

  • Animals, Newborn
  • Bronchopulmonary Dysplasia
  • Hyperoxia
  • Hypoxia

abstract

  • Premature infants with lung injury often experience intermittent episodes of hypoxemia. This study investigates whether intermittent hypoxemia exacerbates oxidative stress and lung injury in neonatal mice in a hyperoxia-induced model of bronchopulmonary dysplasia (BPD). For the BPD model, 3-day-old C57Bl/6J mice were exposed to hyperoxia (65% O(2)) for 4 weeks (O(2) group) or to hyperoxia and intermittent (10 min daily) hypoxia (O(2) + H group). Upon completion of O(2) or O(2) + H exposure, the degree of pulmonary alveolarization and granulocytic infiltration were examined. The severity of oxidative injury in lungs was defined by tissue glutathione and protein carbonyl content. Data were compared to those in naïve mice and mice subjected only to intermittent hypoxia. Hyperoxia-exposed mice exhibited a dramatic (p < 0.0001) decrease of alveolarization, significantly increased granulocytic infiltration (p < 0.0001) and increased protein carbonyl content (p = 0.04) compared to naïve mice. However, O(2) + H mice demonstrated significantly (p = 0.03) fewer alveoli compared to their O(2) counterparts. This was associated with a significantly (p = 0.02) decreased pulmonary total/oxidized glutathione ratio and a significant (p = 0.03) elevation of protein carbonyl content. Thus, intermittent hypoxic stress during hyperoxic induction of BPD in mice potentiates oxidative stress in lung tissue and exacerbates alveolar developmental arrest. (c) 2008 S. Karger AG, Basel.

publication date

  • 2009

has subject area

  • Animals
  • Animals, Newborn
  • Bronchopulmonary Dysplasia
  • Disease Models, Animal
  • Female
  • Glutathione
  • Humans
  • Hyperoxia
  • Hypoxia
  • Infant, Newborn
  • Lung
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Oxidative Stress
  • Oxygen
  • Protein Carbonylation
  • Pulmonary Alveoli

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed Central ID

  • PMC3659784

Digital Object Identifier (DOI)

  • 10.1159/000178798

PubMed ID

  • 19052476

Additional Document Info

start page

  • 299

end page

  • 305

volume

  • 95

number

  • 4