Inhibition of arachidonic acid metabolism is not involved in dexamethasone-induced growth inhibition in embryonic palatal development.
Previous studies have shown that glucocorticoids induce cleft palate in susceptible strains of mice and inhibit proliferation of palatal mesenchyme cells in vivo and in culture. The present study shows that the synthetic glucocorticoid, dexamethasone (DEX), inhibits serum-stimulated arachidonic acid release in cultured mouse palatal mesenchyme cells. Arachidonic acid could neither prevent the DEX effect on cell proliferation when added in culture nor prevent glucocorticoid-induced cleft palate when administered in vivo. Furthermore, the time course for DEX-induced inhibition of arachidonic acid release (maximal by 5h) is markedly different from the time courses for both inhibition of cell proliferation in culture and cleft palate induction in vivo (3 to 4 days). These results suggest that both DEX-induced cleft palate formation and inhibition of palatal cell proliferation arise from some mechanism other than a DEX-induced inhibition of arachidonic acid metabolism.
D000818:Animals; D001095:Arachidonic Acids / Q000037:antagonists & inhibitors / Q000378:metabolism*; D002478:Cells, Cultured; D002972:Cleft Palate / Q000139:chemically induced; D003907:Dexamethasone / Q000494:pharmacology*; D006854:Hydrocortisone / Q000633:toxicity; D051379:Mice; D010159:Palate / Q000187:drug effects / Q000196:embryology*; D011453:Prostaglandins / Q000096:biosynthesis; D014222:Triamcinolone Acetonide / Q000031:analogs & derivatives / Q000633:toxicity
D001095:Arachidonic Acids; D011453:Prostaglandins; D003907:Dexamethasone; D014222:Triamcinolone Acetonide; C005900:triamcinolone hexacetonide; D006854:Hydrocortisone