Role of oxidant injury in the pathogenesis of neonatal lung disease

被引:38
作者
Davis, JM [1 ]
机构
[1] SUNY Stony Brook, Winthrop Univ Hosp, Sch Med, Div Neonatol, Mineola, NY 11501 USA
关键词
antioxidant; bronchopulmonary dysplasia; oxygen radicals; superoxide dismutase;
D O I
10.1080/08035250260095762
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that develops in newborn infants treated with oxygen and mechanical ventilation for a primary lung disorder. With significant improvements in survival of many critically ill infants, BPD has become an extremely important complication of newborn intensive care. The pathogenesis of BPD is complex and involves a variety of causative factors. However, increasing evidence has suggested that an oxidative insult could be an extremely important component of the injury process. Premature infants are especially sensitive to oxidant injury since they are exposed to supraphysiological concentrations of oxygen at birth while endogenous antioxidant enzyme activity may be relatively deficient. Conclusion: Superoxide dismutase is an antioxidant enzyme that has been shown in numerous basic and clinical studies to protect cells against oxidant injury.
引用
收藏
页码:23 / 25
页数:3
相关论文
共 26 条
[1]  
[Anonymous], EFFECTIVE CARE NEWBO
[2]   INCREASED ACTIVITY OF INTERLEUKIN-6 BUT NOT TUMOR-NECROSIS-FACTOR-ALPHA IN LUNG LAVAGE OF PREMATURE-INFANTS IS ASSOCIATED WITH THE DEVELOPMENT OF BRONCHOPULMONARY DYSPLASIA [J].
BAGCHI, A ;
VISCARDI, RM ;
TACIAK, V ;
ENSOR, JE ;
MCCREA, KA ;
HASDAY, JD .
PEDIATRIC RESEARCH, 1994, 36 (02) :244-252
[3]   NEURODEVELOPMENTAL OUTCOME IN INFANTS WITH BRONCHOPULMONARY DYSPLASIA [J].
BREGMAN, J ;
FARRELL, EE .
CLINICS IN PERINATOLOGY, 1992, 19 (03) :673-694
[4]   MICE LACKING EXTRACELLULAR-SUPEROXIDE DISMUTASE ARE MORE SENSITIVE TO HYPEROXIA [J].
CARLSSON, LM ;
JONSSON, J ;
EDLUND, T ;
MARKLUND, SL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (14) :6264-6268
[5]   Intracellular uptake of recombinant superoxide dismutase after intratracheal administration [J].
Das, S ;
Horowitz, S ;
Robbins, CG ;
El-Sabban, ME ;
Sahgal, N ;
Davis, JM .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1998, 274 (05) :L673-L677
[6]   Long-term follow-up of premature infants treated with prophylactic, intratracheal recombinant human CuZn superoxide dismutase [J].
Davis J.M. ;
Richter S.E. ;
Biswas S. ;
Rosenfeld W.N. ;
Parton L. ;
Gewolb I.H. ;
Parad R. ;
Carlo W. ;
Couser R.J. ;
Baumgart S. ;
Atluru V. ;
Salerno L. ;
Kassem N. .
Journal of Perinatology, 2000, 20 (4) :213-216
[7]  
Davis JM, 2000, PEDIATR RES, V47, p395A
[8]   Safety and pharmacokinetics of multiple doses of recombinant human CuZn superoxide dismutase administered intratracheally to premature neonates with respiratory distress syndrome [J].
Davis, JM ;
Rosenfeld, WN ;
Richter, SE ;
Parad, R ;
Gewolb, IH ;
Spitzer, AR ;
Carlo, WA ;
Couser, RJ ;
Price, A ;
Flaster, E ;
Kassem, N ;
Edwards, L ;
Tierney, J ;
Horowitz, S .
PEDIATRICS, 1997, 100 (01) :24-30
[9]   PROPHYLACTIC EFFECTS OF RECOMBINANT HUMAN SUPEROXIDE-DISMUTASE IN NEONATAL LUNG INJURY [J].
DAVIS, JM ;
ROSENFELD, WN ;
SANDERS, RJ ;
GONENNE, A .
JOURNAL OF APPLIED PHYSIOLOGY, 1993, 74 (05) :2234-2241
[10]  
Davis JM, 1999, NEONATOLOGY, P509