The effect of prenatal dexamethasone on fetal rat lung prostaglandin synthesis

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

doi:10.1016/0262-1746(83)90017-3

The effect of prenatal dexamethasone on fetal rat lung prostaglandin synthesis

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

Laboratory Medicine and Pathology

Research output: Contribution to journal › Article › peer-review

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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_1α (6-keto-PGF_1α), prostaglandin E₂ (PGE₂), and 12-L-hydroxy-5,8,10-heptadecatrienoic acid (HHT). Prostaglandin F_2α, (PGF_2α), 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_1α, 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 language	English (US)
Pages (from-to)	171-177
Number of pages	7
Journal	Prostaglandins, Leukotrienes and Medicine
Volume	11
Issue number	2
DOIs	https://doi.org/10.1016/0262-1746(83)90017-3
State	Published - 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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title = "The effect of prenatal dexamethasone on fetal rat lung prostaglandin synthesis",

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 F1α (6-keto-PGF1α), prostaglandin E2 (PGE2), and 12-L-hydroxy-5,8,10-heptadecatrienoic acid (HHT). Prostaglandin F2α, (PGF2α), 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-PGF1α, 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.",

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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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AU - Josephson, Mark W.

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AU - Brown, David M.

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N2 - [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 F1α (6-keto-PGF1α), prostaglandin E2 (PGE2), and 12-L-hydroxy-5,8,10-heptadecatrienoic acid (HHT). Prostaglandin F2α, (PGF2α), 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-PGF1α, 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.

AB - [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 F1α (6-keto-PGF1α), prostaglandin E2 (PGE2), and 12-L-hydroxy-5,8,10-heptadecatrienoic acid (HHT). Prostaglandin F2α, (PGF2α), 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-PGF1α, 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.

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The effect of prenatal dexamethasone on fetal rat lung prostaglandin synthesis

Abstract

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