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

Michael Y Tsai, S. Einzig

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)25-30
Number of pages6
JournalProstaglandins, Leukotrienes and Essential Fatty Acids
Volume38
Issue number1
DOIs
StatePublished - Oct 1989

Bibliographical note

Funding Information:
expert technical assistanceT. his study was supportedb y a grant from the American Heart Association, Minnesota Affiliate.

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