Document Detail


Oxidative stress in lavage fluid of preterm infants at risk of chronic lung disease.
MedLine Citation:
PMID:  11704534     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
There is evidence that oxidative stress plays a role in the development of chronic lung disease (CLD), with immature lungs being particularly sensitive to the injurious effect of oxygen and mechanical ventilation. We analyzed total ascorbate, urate, and protein carbonyls in 102 bronchoalveolar lavage fluid samples from 38 babies (33 preterm, 24-36 wk gestation; 5 term, 37-39 wk gestation). Preterm babies had significantly decreasing concentrations of ascorbate, urate, and protein carbonyls during the first 9 days of life (days 1-3, 4-6, and 7-9, Kruskal-Wallis ANOVA: P = 0.016, P < 0.0001, and P = 0.010, respectively). Preterm babies had significantly higher protein carbonyl concentrations at days 1-3 and 4-6 (P = 0.005 and P = 0.044) compared with term babies. Very preterm babies (24-28 wk gestation) had increased concentrations of protein carbonyls at days 4-6 (P = 0.056) and significantly decreased ascorbate concentrations at days 4-6 (P = 0.004) compared with preterm babies (29-36 wk gestation). Urate concentrations were significantly elevated at days 1-3 (P = 0.023) in preterm babies who subsequently developed CLD. This study has shown the presence of oxidative stress in the lungs of preterm babies during ventilation, especially in those who subsequently developed CLD.
Authors:
B C Schock; D G Sweet; H L Halliday; I S Young; M Ennis
Related Documents :
16741334 - Noma neonatorum.
11529384 - Growth and development of children conceived by intracytoplasmic sperm injection at kin...
7070334 - Newborn transport in south australia, 1978-80: experience of the queen victoria hospita...
10531914 - Motherhood: the emotional awakening.
19930634 - Bronchoalveolar lavage fluid from preterm infants with chorioamnionitis inhibits alveol...
10823884 - Maternal sdf1 3'a polymorphism is associated with increased perinatal human immunodefic...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  281     ISSN:  1040-0605     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2001 Dec 
Date Detail:
Created Date:  2001-11-12     Completed Date:  2002-01-17     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L1386-91     Citation Subset:  IM    
Affiliation:
Department of Clinical Biochemistry, The Queen's University of Belfast, Belfast BT12 6BJ, United Kingdom.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Antioxidants / analysis
Ascorbic Acid / analysis
Biological Markers
Bronchoalveolar Lavage Fluid / chemistry*
Chronic Disease
Female
Humans
Infant, Newborn
Infant, Premature / metabolism*
Lung / growth & development,  metabolism
Lung Diseases / epidemiology,  metabolism*,  therapy
Male
Oxidation-Reduction
Oxidative Stress
Proteins / metabolism
Respiration, Artificial
Risk Factors
Treatment Outcome
Uric Acid / analysis
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Biological Markers; 0/Proteins; 50-81-7/Ascorbic Acid; 69-93-2/Uric Acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Oxygen-induced fetal pulmonary vasodilation is mediated by intracellular calcium activation of K(Ca)...
Next Document:  Acute cigarette smoke exposure induces apoptosis of alveolar macrophages.