title: Early high dose antioxidant vitamins do not prevent bronchopulmonary dysplasia in premature baboons exposed to prolonged hyperoxia: a pilot study.
abstract: The antioxidant vitamins ascorbic acid (AA) and alpha-tocopherol (alpha-TP) effectively inhibit oxygen free radical-induced lipid peroxidation. Using a premature baboon model of hyperoxia-induced bronchopulmonary dysplasia (BPD), we measured concentrations of AA, alpha-TP, and conjugated dienes (CD, marker of lipid peroxidation) in four animals (hyperoxic antioxidant group) receiving high dose antioxidant vitamin supplementation (AA, 100 mg x kg x(-1) x d(-1); alpha-TP; 20 mg x kg x(-1) x d(-1)) and one animal receiving standard dose antioxidant vitamin supplementation (AA, 10 mg x kg x(-1) x d(-1); alpha-TP, 1 mg x kg x(-1) x d(-1)). Respiratory and histopathologic data were compared with data from 10 historical animals exposed to hyperoxia (hyperoxic control group) and 11 historical animals treated as required with oxygen (normoxic control group) who had received standard dose antioxidant vitamin supplementation. Compared with standard dose antioxidant vitamin supplementation, high dose antioxidant vitamin supplementation effectively raised AA concentrations in plasma (37 +/- 22 micromol/L and 395 +/- 216 micromol/L, respectively) and tracheal aspirates (62 +/- 35 micromol/L and 286 +/- 205 micromol/L, respectively), and alpha-TP concentrations in plasma (10.1 +/- 2.5 micromol/L and 24.6 +/- 17.5 micromol/L, respectively). However, there was no apparent effect on tracheal aspirate CD concentrations (482 +/- 333 micromol/L and 1050 +/- 1111 micromol/L, respectively), and respiratory parameters in the hyperoxic antioxidant group were comparable to those of the hyperoxic control group but significantly worse than in the normoxic control group. Finally, no protective effect of high dose antioxidant vitamin supplementation was noted at the histopathologic level.
authors.affiliation: Joint Program in Neonatology, Harvard Medical School, Boston, Massachusetts 02115, USA.
authors.forename: T M
authors.initials: TM
authors.lastname: Berger
authors.forename: B
authors.initials: B
authors.lastname: Frei
authors.forename: N
authors.initials: N
authors.lastname: Rifai
authors.forename: M E
authors.initials: ME
authors.lastname: Avery
authors.forename: J
authors.initials: J
authors.lastname: Suh
authors.forename: B A
authors.initials: BA
authors.lastname: Yoder
authors.forename: J J
authors.initials: JJ
authors.lastname: Coalson
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D000975:Antioxidants / Q000627:therapeutic use*; D001997:Bronchopulmonary Dysplasia / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D005865:Gestational Age; D006801:Humans; D018496:Hyperoxia; D007231:Infant, Newborn; D008168:Lung / Q000187:drug effects / Q000473:pathology*; D010215:Papio; D010865:Pilot Projects; D012044:Regression Analysis; D014810:Vitamin E / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; D014810:Vitamin E