Prostaglandin catabolism in fetal and maternal tissues - A study of 15-hydroxyprostaglandin dehydrogenase and Δ13 reductase with specific assay methods

Recent studies have demonstrated that extraductal tissues such as lung are important sources of prostaglandin E₂ which maintains the patency of ductus arteriosus in fetuses and prematurely-born infants. Also, organs such as lung are known to be active in the catabolism of PGE₂. Earlier studies of enzymes involved in the catabolism of PGE₂ such as 15-hydroxyprostaglandin dehydrogenase (15-PGDH) and Δ13 reductase all used non-specific methods. In the present report, we studied 15-PGDH in fetal and maternal rat lung, kidney, and fetal lamb lung, kidney and ductus arteriosus with the use of a specific substrate (15-S)-[15³H-PGE₂]. In addition, we measured the activity of Δ13 reductase in these tissues by measuring the conversion of [1-¹⁴C]-15-keto PGE₂ to [1-¹⁴C]-15-keto-13,14-dihydro PGE₂. The results from these studies demonstrated that in fetal rat lung and kidney, 15-PGDH activities increased rapidly while Δ13 reductase remained unchanged during late gestation. Ductus arteriosus possessed little 15-PGDH activities. These results strongly suggest that extraductal regulation of PGE₂ metabolism is important in determining ductal caliber in fetuses and prematurely delivered neonates.