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RECORD NUMBER: 6 OF 10

Main Title Fetal Dexamethasone Exposure Impairs Cellular Development in Neonatal Rat Heart and Kidney: Effects on DNA and Protein in Whole Tissues.
Author Slotkin, T. A. ; Seidler, F. J. ; Kavlock, R. J. ; Bartolome., J. V. ;
CORP Author Duke Univ. Medical Center, Durham, NC. Dept. of Pharmacology.;Health Effects Research Lab., Research Triangle Park, NC. Developmental Toxicology Div.
Publisher c1991
Year Published 1991
Report Number EPA-R-813769; EPA/600/J-91/179;
Stock Number PB91-233429
Additional Subjects Dexamethasone ; Prenatal exposure delayed effects ; Heart ; Kidney ; Deoxyribonucleic acids ; Toxicity ; Proteins ; Glucocorticoids ; Fetus ; Rats ; Mitosis ; Reprints ;
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NTIS  PB91-233429 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 7p
Abstract
Fetal glucocorticoid exposure causes postnatal growth retardation. To examine the mechanisms underlying effects on specific organ systems, the authors administered 0.2 or 0.8 mg/kg of dexamethasone to pregnant rats on gestational days 17, 18, and 19 and assessed three biochemical markers of cell development in heart and kidney of the offspring: DNA content per organ as an index of total cell numbers, DNA per g tissue as an index of cell packing density, and protein/DNA ratio as an index of relative cell size. In both tissues, DNA content became markedly subnormal during the first postnatal week, theontogenetic period of rapid cell division. Partial recovery occurred by the end of the first postnatal month. In the heart, cell packing density was subnormal initially and the cells were significantly enlarged. In contrast, packing density was slightly elevated in the kidney; protein/DNA was increased by the low dose of dexamethasone, but markedly decreased by the high dose. (Copyright (c) 1991 Wiley-Liss, Inc.)