Oral docosahexaenoic acid given to pregnant mice increases the amount of surfactant in lung and amniotic fluid in preterm fetuses

Paola G. Blanco, Steven D. Freedman, Mari C. Lopez, Mario Ollero, Elizabeth Comen, Michael Laposata, Juan G. Alvarez

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Objective: Our purpose was to determine whether docosahexaenoic acid increased surfactant production, as reflected by increased dipalmitoyl phosphatidylcholine, in mouse fetal lung and amniotic fluid. Study design: On day 9.5 of gestation, pregnant mice were given docosahexaenoic acid orally at 0, 5, 10, or 20 mg per day and were killed at day 16.5 (preterm) and day 19.5 (term) of gestation. Dipalmitoyl phosphatidylcholine was measured in fetal lung homogenates and amniotic fluid by high-performance thin-layer chromatography. Results: Dipalmitoyl phosphatidylcholine values in lung were 0.22 ± 0.27 μg/mg of total protein in preterm versus 1.96 ± 0.57 μg/mg in term control fetuses. Pretreatment with 5, 10, or 20 mg docosahexaenoic acid increased dipalmitoyl phosphatidylcholine levels in preterm fetuses to 1.20 ± 0.75, 1.60 ± 0.67, and 3.28 ± 0.44 μg/mg of protein, respectively. A similar trend was observed in amniotic fluid in which dipalmitoyl phosphatidylcholine levels were 1.86 ± 3.70 μg/ mL in preterm fetuses at baseline and increased to 7.81 ± 1.21, 16.83 ± 1.62 and 22.72 ± 3.44 μg/mL after pretreatment for 7 days with 5, 10, and 20 mg docosahexaenoic acid (P < .05 compared to untreated mice). Dipalmitoyl phosphatidylcholine levels in amniotic fluid were 24.46 ± 10.3 μg/mL in term control mice. Conclusion: The oral administration of docosahexaenoic acid to pregnant mice during pregnancy can induce dipalmitoyl phosphatidylcholine production and secretion, which is the major lipid component of surfactant.

Original languageEnglish (US)
Pages (from-to)1369-1374
Number of pages6
JournalAmerican Journal of Obstetrics and Gynecology
Volume190
Issue number5
DOIs
StatePublished - May 2004
Externally publishedYes

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1,2-Dipalmitoylphosphatidylcholine
Docosahexaenoic Acids
Amniotic Fluid
Surface-Active Agents
Fetus
Lung
Pregnancy
Thin Layer Chromatography
Oral Administration
Proteins
Lipids

Keywords

  • Docosahexaenoic acid
  • Respiratory distress syndrome
  • Surfactant

ASJC Scopus subject areas

  • Medicine(all)
  • Obstetrics and Gynecology

Cite this

Oral docosahexaenoic acid given to pregnant mice increases the amount of surfactant in lung and amniotic fluid in preterm fetuses. / Blanco, Paola G.; Freedman, Steven D.; Lopez, Mari C.; Ollero, Mario; Comen, Elizabeth; Laposata, Michael; Alvarez, Juan G.

In: American Journal of Obstetrics and Gynecology, Vol. 190, No. 5, 05.2004, p. 1369-1374.

Research output: Contribution to journalArticle

Blanco, Paola G. ; Freedman, Steven D. ; Lopez, Mari C. ; Ollero, Mario ; Comen, Elizabeth ; Laposata, Michael ; Alvarez, Juan G. / Oral docosahexaenoic acid given to pregnant mice increases the amount of surfactant in lung and amniotic fluid in preterm fetuses. In: American Journal of Obstetrics and Gynecology. 2004 ; Vol. 190, No. 5. pp. 1369-1374.
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abstract = "Objective: Our purpose was to determine whether docosahexaenoic acid increased surfactant production, as reflected by increased dipalmitoyl phosphatidylcholine, in mouse fetal lung and amniotic fluid. Study design: On day 9.5 of gestation, pregnant mice were given docosahexaenoic acid orally at 0, 5, 10, or 20 mg per day and were killed at day 16.5 (preterm) and day 19.5 (term) of gestation. Dipalmitoyl phosphatidylcholine was measured in fetal lung homogenates and amniotic fluid by high-performance thin-layer chromatography. Results: Dipalmitoyl phosphatidylcholine values in lung were 0.22 ± 0.27 μg/mg of total protein in preterm versus 1.96 ± 0.57 μg/mg in term control fetuses. Pretreatment with 5, 10, or 20 mg docosahexaenoic acid increased dipalmitoyl phosphatidylcholine levels in preterm fetuses to 1.20 ± 0.75, 1.60 ± 0.67, and 3.28 ± 0.44 μg/mg of protein, respectively. A similar trend was observed in amniotic fluid in which dipalmitoyl phosphatidylcholine levels were 1.86 ± 3.70 μg/ mL in preterm fetuses at baseline and increased to 7.81 ± 1.21, 16.83 ± 1.62 and 22.72 ± 3.44 μg/mL after pretreatment for 7 days with 5, 10, and 20 mg docosahexaenoic acid (P < .05 compared to untreated mice). Dipalmitoyl phosphatidylcholine levels in amniotic fluid were 24.46 ± 10.3 μg/mL in term control mice. Conclusion: The oral administration of docosahexaenoic acid to pregnant mice during pregnancy can induce dipalmitoyl phosphatidylcholine production and secretion, which is the major lipid component of surfactant.",
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T1 - Oral docosahexaenoic acid given to pregnant mice increases the amount of surfactant in lung and amniotic fluid in preterm fetuses

AU - Blanco, Paola G.

AU - Freedman, Steven D.

AU - Lopez, Mari C.

AU - Ollero, Mario

AU - Comen, Elizabeth

AU - Laposata, Michael

AU - Alvarez, Juan G.

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N2 - Objective: Our purpose was to determine whether docosahexaenoic acid increased surfactant production, as reflected by increased dipalmitoyl phosphatidylcholine, in mouse fetal lung and amniotic fluid. Study design: On day 9.5 of gestation, pregnant mice were given docosahexaenoic acid orally at 0, 5, 10, or 20 mg per day and were killed at day 16.5 (preterm) and day 19.5 (term) of gestation. Dipalmitoyl phosphatidylcholine was measured in fetal lung homogenates and amniotic fluid by high-performance thin-layer chromatography. Results: Dipalmitoyl phosphatidylcholine values in lung were 0.22 ± 0.27 μg/mg of total protein in preterm versus 1.96 ± 0.57 μg/mg in term control fetuses. Pretreatment with 5, 10, or 20 mg docosahexaenoic acid increased dipalmitoyl phosphatidylcholine levels in preterm fetuses to 1.20 ± 0.75, 1.60 ± 0.67, and 3.28 ± 0.44 μg/mg of protein, respectively. A similar trend was observed in amniotic fluid in which dipalmitoyl phosphatidylcholine levels were 1.86 ± 3.70 μg/ mL in preterm fetuses at baseline and increased to 7.81 ± 1.21, 16.83 ± 1.62 and 22.72 ± 3.44 μg/mL after pretreatment for 7 days with 5, 10, and 20 mg docosahexaenoic acid (P < .05 compared to untreated mice). Dipalmitoyl phosphatidylcholine levels in amniotic fluid were 24.46 ± 10.3 μg/mL in term control mice. Conclusion: The oral administration of docosahexaenoic acid to pregnant mice during pregnancy can induce dipalmitoyl phosphatidylcholine production and secretion, which is the major lipid component of surfactant.

AB - Objective: Our purpose was to determine whether docosahexaenoic acid increased surfactant production, as reflected by increased dipalmitoyl phosphatidylcholine, in mouse fetal lung and amniotic fluid. Study design: On day 9.5 of gestation, pregnant mice were given docosahexaenoic acid orally at 0, 5, 10, or 20 mg per day and were killed at day 16.5 (preterm) and day 19.5 (term) of gestation. Dipalmitoyl phosphatidylcholine was measured in fetal lung homogenates and amniotic fluid by high-performance thin-layer chromatography. Results: Dipalmitoyl phosphatidylcholine values in lung were 0.22 ± 0.27 μg/mg of total protein in preterm versus 1.96 ± 0.57 μg/mg in term control fetuses. Pretreatment with 5, 10, or 20 mg docosahexaenoic acid increased dipalmitoyl phosphatidylcholine levels in preterm fetuses to 1.20 ± 0.75, 1.60 ± 0.67, and 3.28 ± 0.44 μg/mg of protein, respectively. A similar trend was observed in amniotic fluid in which dipalmitoyl phosphatidylcholine levels were 1.86 ± 3.70 μg/ mL in preterm fetuses at baseline and increased to 7.81 ± 1.21, 16.83 ± 1.62 and 22.72 ± 3.44 μg/mL after pretreatment for 7 days with 5, 10, and 20 mg docosahexaenoic acid (P < .05 compared to untreated mice). Dipalmitoyl phosphatidylcholine levels in amniotic fluid were 24.46 ± 10.3 μg/mL in term control mice. Conclusion: The oral administration of docosahexaenoic acid to pregnant mice during pregnancy can induce dipalmitoyl phosphatidylcholine production and secretion, which is the major lipid component of surfactant.

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KW - Respiratory distress syndrome

KW - Surfactant

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