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The Regulation of Arachidonic Acid Release in Parturition

  • John M. Johnston
  • Dennis R. Hoffman
Part of the NATO ASI Series book series (NSSA, volume 116)

Abstract

One of the rate limiting steps in prostaglandin biosynthesis is the release of free arachidonic acid (1,2). In the present investigation is described the results of a study in which: 1) we have defined the lipid species of the human fetal membranes that serves as the source of arachidonic acid for prostaglandin biosynthesis during human parturition; 2) we have defined the enzymatic mechanism involved in this release; 3) we have investigated the regulation of these processes with special emphasis on the possible inter-relationship between the fetal lung and fetal membranes, to the initiation of parturition. Several years ago we observed that the concentration of arachidonic acid increased disproportionally in human amniotic fluid during labor (3). It has been reported by numerous investigators that prostaglandins are produced in large amounts by uterine and intra-uterine tissues during parturition. We also demonstrated that the microsomal fraction prepared from several intra-uterine tissues, including amnion, and chorion laeve, had a high capacity for prostaglandin formation from arachidonic acid (4). We suggested that the source of the arachidonic acid was fetal membranes.

Keywords

Arachidonic Acid Lamellar Body Fetal Membrane Arachidonic Acid Release Arachidonic Acid Content 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • John M. Johnston
    • 1
  • Dennis R. Hoffman
    • 1
  1. 1.Departments of Biochemistry and Obstetrics-Gynecology and The Cecil H. and Ida Green Center for Reproductive Biology SciencesThe University of Texas Health Science Center at DallasDallasUSA

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