Record Display for the EPA National Library Catalog


OLS Field Name OLS Field Data
Main Title Control of Alkaline Phosphatase Activity in C3H10T1/2 Cells: Role of Retinoic Acid and Cell Density.
Author Reese, D. H. ; Larsen, R. A. ; Hornicek, F. J. ;
CORP Author Environmental Protection Agency, Washington, DC. Office of Health and Environmental Assessment. ;AScI Corp., McLean, VA.
Publisher cSep 91
Year Published 1991
Report Number EPA/600/J-92/239 ;OHEA-R-447;
Stock Number PB92-198639
Additional Subjects Tretinoin ; Alkaline phosphatase ; Cells(Biology) ; Mice ; Neoplasms ; Serum-free media ; Up-regulation(Physiology) ; Enzyme induction ; Dose-response relationships ; Reprints ;
Library Call Number Additional Info Location Last
NTIS  PB92-198639 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 06/01/1993
Collation 12p
The authors have begun to use the chemically-transformable mouse embryo fibroblast cell, C3H10T1/2, to investigate that altered AP expression in some cancers may be caused by a defect in the ability of the cells to respond normally to retinoid. In the initial study they characterized AP regulation in normal C3H10T1/2 cells and show that: (1) RA increases AP activity within 3-4 h in serum-free medium; (2) serum inhibits short-term induction (0-8 h) in a concentration-dependent manner (10% serum causes complete inhibition); (3) during long-term RA exposure (24 h and 48 h), induction can be detected in serum-containing medium; (d) AP induction is dose related in serum-free medium; (5) ten to the minus fifth power M RA is ineffective at inducing AP in serum-free medium during 8 h but is the most effective concentration in serum-containing medium during 24 h and 48 h exposures; (6) AP inducibility by RA requires near-confluent cell densities; and, (7) when cultures become confluent, cells become constitutive for AP and no longer require RA for enzyme expression.