Early protein oxidation in the neonatal lung is related to development of chronic lung disease

Acta Paediatr. 1995 Nov;84(11):1296-9. doi: 10.1111/j.1651-2227.1995.tb13552.x.


Free radical-mediated oxidation of proteins may impair their function and cause cellular damage. We studied pulmonary protein oxidation and its association with the development of chronic lung disease in 61 newborn infants (mean gestational age 31.1 +/- 4.0, range 24-41 weeks) requiring intensive care with oxygen therapy. Protein oxidation was quantified as protein carbonylation in tracheal aspirates recovered daily during the first week of life. Mean carbonyl concentration was 3.5 +/- 1.6 mumol/mg protein. Negative correlations existed between protein carbonylation during days 2-4 and gestational age (day 2: r = -0.37, p = 0.01; day 3: r = -0.48, p = 0.001; and day 4: r = -0.33, p = 0.03). Patients who developed bronchopulmonary dysplasia showed significantly higher protein carbonylation on days 1-6 (all p < 0.05). In multiple regression analysis explaining bronchopulmonary dysplasia, using gestational age, inspired oxygen on days 1-3 and protein carbonylation on day 3 as independent variables, only protein carbonylation remained significant. We conclude that immaturity is the most important factor explaining free radical-mediated pulmonary protein oxidation in newborn infants and that oxidation of proteins is related to the development of chronic lung disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bronchopulmonary Dysplasia / diagnosis*
  • Bronchopulmonary Dysplasia / therapy
  • Chronic Disease
  • Female
  • Free Radicals
  • Gestational Age
  • Humans
  • Infant, Newborn
  • Infant, Premature
  • Lipid Peroxidation
  • Male
  • Oxidative Stress
  • Oxygen / therapeutic use
  • Proteins / analysis*


  • Free Radicals
  • Proteins
  • Oxygen