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Main Title Prenatal Dexamethasone Administration Disrupts the Pattern of Cellular Development in Rat Lung.
Author Navarro, H. A. ; Kudlacz, E. M. ; Eylers, J. P. ; Slotkin, T. A. ;
CORP Author Duke Univ. Medical Center, Durham, NC. Dept. of Pharmacology.;Health Effects Research Lab., Research Triangle Park, NC.
Publisher c1989
Year Published 1989
Report Number EPA-R-813769; EPA/600/J-89/377;
Stock Number PB90-216227
Additional Subjects Lung ; Toxicology ; Graphs(Charts) ; Deoxyribonucleic acids ; Rats ; Proteins ; Gestation ; Cell division ; Reprints ; Dexamethasone ; Prenatal exposure delayed effects ; Organ weight ; Ornithine decarboxylase ; Beta adrenergic receptors ; Cell differentiation ; Isoproterenol
Library Call Number Additional Info Location Last
NTIS  PB90-216227 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 8p
To examine whether prenatal exposure to glucocorticoids could adversely affect subsequent cellular development of the lung, the authors administered 0.2 mg/kg of dexamethasone to pregnant rats on gestational days 17, 18, and 19. Lungs of the offspring were then examined for patterns of cell acquisition (DNA) and growth (protein). DNA concentration (a marker of cell packing density) and DNA content (a measure of total cell numbers) were reduced during gestation, and the shortfalls in concentration persisted past weaning. Disruption of development was also apparent in the protein/DNA ratio, which was consistently elevated, a finding consistent with cellular hypertrophy. In addition, lung ornithine decarboxylase became coupled to beta-adrenergic receptors prematurely in the dexamethasone group, suggesting that neural control of tissue differentiation is altered. These data indicate that prenatal glucocorticoids may compromise lung development through effects on cell replication and differentiation, which derive, in part, from alterations in the reception of trophic neural signals. (Copyright (c) 1989 Alan R. Liss, Inc.)