Diminished PGE<emph type="8">2 content, enhanced PGE<emph type="8">2 release and defects in <emph type="7">3H-PGE<emph type="8">2 transport in embryos from overtly diabetic rats

Abstract

Diminished PGE<emph type="8">2 levels in diabetic embryos are relatedto the development of malformations, and thus the aim of the present study wasto determine whether PGE<emph type="8">2 levels are modified in ratembryos cultured in diabetic serum during organogenesis, and ifPGE<emph type="8">2 content and release, and<emph type="7">3H-PGE<emph type="8">2 uptake and release, arealtered in incubated diabetic embryos. Rats were made diabetic bysteptozotocin (60 mg kg<emph type="7">-1) before mating. Controlrat embryos cultured for 24 h (explantation Day 9) in the presence of diabeticserum showed diminished PGE<emph type="8">2 levels. When Day 10diabetic embryos were incubated, embryo PGE<emph type="8">2 levels werelower, but the PGE<emph type="8">2 released to the incubation media wasmuch higher than in controls. Uptake of<emph type="7">3H-PGE<emph type="8">2 by diabetic embryos wasinitially enhanced (5-10 min), then reached similar levels to controls(20-100 min). Release of<emph type="7">3H-PGE<emph type="8">2 previously incorporatedduring a 60-min incubation was greater in diabetic embryos than in controls.These results show diminished PGE<emph type="8">2 content in bothdiabetic and normal embryos cultured in the presence of diabetic serum, butsuggest that diabetic embryos have the capability to produce and release highlevels of PGE<emph type="8">2. The enhanced release ofPGE<emph type="8">2 is probably the result of transport abnormalities,and leads to the elevated PGE<emph type="8">2 concentrations found inthe incubating medium and to the diminished intraembryonicPGE<emph type="8">2 levels that alter embryonic development.