The effect of prenatal dexamethasone on fetal rat lung prostaglandin synthesis

Michael Y Tsai, Mark W. Josephson, Bill Handschin, David M. Brown

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

[14C]Arachidonic acid conversions were studied in homogenates of lungs from 20, 21, and 22 day fetuses with or without prenatal dexamethasone treatment. The major metabolites were in all cases 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE), 6-keto-prostaglandin F (6-keto-PGF), prostaglandin E2 (PGE2), and 12-L-hydroxy-5,8,10-heptadecatrienoic acid (HHT). Prostaglandin F, (PGF), prostaglandin D2 (PGD2), and thromboxane B2 (TxB2) were present in small amounts. Dexamethasone treatment significantly stimulated the conversion of [14C]-arachidonic acid in fetal lung homogenates to 6-keto-PGF, PGE2, 12-HETE, and HHT, at 20 days gestational age. This effect was dependent on the dose of dexamethasone. These results suggest that dexamethasone accelerates the maturation of the enzymes involved in prostaglandin synthesis. Because dexamethasone is also known to inhibit phospholipase A2, further studies are required to determine the overall in vivo effect of prenatal dexamethasone therapy on fetal lung prostaglandin synthesis.

Original languageEnglish (US)
Pages (from-to)171-177
Number of pages7
JournalProstaglandins, Leukotrienes and Medicine
Volume11
Issue number2
DOIs
StatePublished - Jun 1983

Bibliographical note

Funding Information:
The authors wish to thank Brad Syverson and Barbara Jensen for their expert technical assistance. This study was supported in part by grants from the Juvenile Diabetes Foundation (79Rl39), the Vikings Children's Fund, and the NIH Biomedical Research Support Grant Program (M.Y.T.), and NIH grant AM-17697 (D.M.B.).

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