Effects of dexamethasone on fetal mouse development.
The in vitro incorporation of 14C-leucine, 3H-uridine and 3H-thymidine into the acid-insoluble components of mouse fetal liver, gut, heart and lung as followed on gestational days 14, 16 and 19. Liver and gut showed a similar pattern: the incoporation of all three substrates decreased steadily until day 19, falling from one tenth to one fifth the values on day 14. Heart and lung decreased by half after day 16. Injection of mothers 16 h earlier with 200 microgram dexamethasone decreased in vitro incorporation on day 14 into liver and gut, respectively, of leucine by 38 and 37% and of thymidine by 67 and 56%. In heart and lung, only thymidine was decreased at this time by 61 and 33%, respectively. Values for uridine were affected significantly only in liver. Thymidine incorporation appeared to be the most sensitive parameter reflecting corticosteroid action and liver the most sensitive tissue. Treated fetuses were born at the usual time and weight gain did not differ from controls over the first 42 days neonatally. It is concluded that dexamethasone accelerates the development of many processes in fetal tissues which are induced by corticosteroids.
D000818:Animals; D003907:Dexamethasone / Q000494:pharmacology*; D005333:Fetus / Q000378:metabolism; D007930:Leucine / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008168:Lung / Q000378:metabolism; D051379:Mice / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism; D013936:Thymidine / Q000378:metabolism; D014529:Uridine / Q000378:metabolism
D003907:Dexamethasone; D007930:Leucine; D013936:Thymidine; D014529:Uridine