A catalytic antioxidant attenuates alveolar structural remodeling in bronchopulmonary dysplasia. Am.J.Respir.Cell Mol.Biol (original) (raw)

2003

Abstract

neuroendocrine cells The pathogenesis of bronchopulmonary dysplasia (BPD) is thought to be multifactorial, with prematurity, barotrauma, inflammation, and pulmonary O2 toxicity playing important roles (1). Evidence suggests that an oxidant/antioxidant im-balance exists in lungs that are at risk for BPD. Higher con-centrations of lipid peroxidation metabolites such as F2-isoprostanes have been found in premature infants (2, 3). Infants who develop BPD have elevated endothelin-1 in tracheal aspirates (4), known to prime both neutrophils and macro-phages to produce more superoxide (5). Preterm babies have lower levels of retinoic acid (6), which has been shown to suppress both superoxide and hydrogen peroxide formation in stimulated neutrophils and macrophages (7). Observations (Received in original form March 20, 2002; accepted in final form September 5, 2002)

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