Fetal dexamethasone exposure impairs cellular development in neonatal rat heart and kidney: effects on DNA and protein in whole tissues.

Published

Journal Article

Fetal glucocorticoid exposure causes postnatal growth retardation. To examine the mechanisms underlying effects on specific organ systems, we 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, the ontogenetic 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. These results suggest that tissue growth impairment caused by prenatal dexamethasone treatment reflects primary deficits in cell proliferation that extend to a variety of different cell types; however, consequent effects on cell packing density and cell size are dose-specific, possibly reflecting actions of glucocorticoids selective for certain cell types or phases of cell development.

Full Text

Duke Authors

Cited Authors

  • Slotkin, TA; Seidler, FJ; Kavlock, RJ; Bartolome, JV

Published Date

  • April 1991

Published In

Volume / Issue

  • 43 / 4

Start / End Page

  • 301 - 306

PubMed ID

  • 2048038

Pubmed Central ID

  • 2048038

International Standard Serial Number (ISSN)

  • 0040-3709

Digital Object Identifier (DOI)

  • 10.1002/tera.1420430404

Language

  • eng

Conference Location

  • United States