Induction of lipid peroxidation of pulmonary surfactant by plasma of preterm babies

Lancet. 1993 Jan 9;341(8837):79-82. doi: 10.1016/0140-6736(93)92557-a.


Respiratory distress syndrome of the preterm baby is believed to be caused by a deficiency of pulmonary surfactant and leakage of plasma into the alveolar spaces. Since the two pathogenetic factors seem to be inter-related, we postulated that peroxidation of surfactant by plasma iron could be the linking mechanism. We obtained cord blood samples from 22 preterm babies (mean gestational age 32.2 [SD 2.7] weeks) and 24 term babies (40.1 [1.6] weeks), and venous blood samples from 18 healthy adults. No adult had detectable non-protein-bound iron in the plasma, but 10/21 (48%) preterm babies and 6/24 (25%) term babies had detectable concentrations (rate difference 23% [95% Cl -5 to 51%], p = 0.20). Transferrin and haptoglobin concentrations were higher and free haemoglobin concentrations lower in adults than in babies (p < 0.005). Only transferrin differed significantly between term and preterm babies. Plasma from all 18 adults and from 23 (96%) term babies inhibited iron-catalysed lipid peroxidation of pulmonary surfactant liposomes. By contrast, plasma from 11 (50%) preterm babies stimulated such peroxidation (difference in stimulation rate 46% [20-71%], p < 0.005 for preterm vs term babies); the ability to stimulate peroxidation was related to the presence of non-protein-bound iron (p < 0.001). Peroxidation decreased in the babies when apotransferrin was added to plasma and in all subjects when alpha-tocopherol was incorporated into the surfactant liposomes. Lipid peroxidation of surfactant may contribute to the pathogenesis of respiratory distress syndrome. Possible therapeutic approaches are increasing babies' iron-binding capacity by plasma transfusions and increasing the antioxidant capacity of commercial surfactant.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Animals
  • Blood Proteins / pharmacology*
  • Humans
  • Infant, Newborn / blood
  • Infant, Premature / blood*
  • Iron / blood
  • Lipid Peroxidation / drug effects*
  • Liposomes
  • Pulmonary Surfactants / drug effects*
  • Spectrophotometry
  • Swine
  • Thiobarbituric Acid Reactive Substances / analysis


  • Blood Proteins
  • Liposomes
  • Pulmonary Surfactants
  • Thiobarbituric Acid Reactive Substances
  • Iron