1977British Journal of PharmacologyOpen access

EFFECT OF p‐BROMOPHENACYL BROMIDE, AN INHIBITOR OF PHOSPHOLIPASE A2, ON ARACHIDONIC ACID RELEASE AND PROSTAGLANDIN SYNTHESIS BY THE GUINEA‐PIG UTERUS in vitro

Sheila M. Mitchell, N.L. Poyser, N.H. Wilson

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Abstract

The synthesis of prostaglandins F2alpha and E2 by guinea-pig uterine homogenates was inhibited by p-bromophenacyl bromide (PBPAB), an inhibitor of phospholipase A2. 2 Metabolism of prostaglandin F2alpha by uterine homogenates was undetectable; this was not affected by PBPAB. 3 There was no significant difference between the amounts of arachidonic acid released from uterine homogenates on days 7 and 1k of the oestrous cycle. Small amounts of dihomo-gamma-linolenic acid were detected in the homogenates. 4 The release of arachidonic acid from uterine homogenates was greatly inhibited by PBPAB. 5 Addition of exogenous arachidonic acid to uterine homogenates did not overcome the inhibition of uterine prostaglandin F2alpha synthesis produced by PBPAB. 6 It is concluded that PBPAB inhibits both the release of arachidonic acid from the guinea-pig uterus and its subsequent conversion into prostaglandins.

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The synthesis of prostaglandins F2alpha and E2 by guinea-pig uterine homogenates was inhibited by p-bromophenacyl bromide (PBPAB), an inhibitor of phospholipase A2. 2 Metabolism of prostaglandin F2alpha by uterine homogenates was undetectable; this was not affected by PBPAB. 3 There was no significant difference between the amounts of arachidonic acid released from uterine homogenates on days 7 and 1k of the oestrous cycle. Small amounts of dihomo-gamma-linolenic acid were detected in the homogenates. 4 The release of arachidonic acid from uterine homogenates was greatly inhibited by PBPAB. 5 Addition of exogenous arachidonic acid to uterine homogenates did not overcome the inhibition of uterine prostaglandin F2alpha synthesis produced by PBPAB. 6 It is concluded that PBPAB inhibits both the release of arachidonic acid from the guinea-pig uterus and its subsequent conversion into prostaglandins.

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Available abstract

The synthesis of prostaglandins F2alpha and E2 by guinea-pig uterine homogenates was inhibited by p-bromophenacyl bromide (PBPAB), an inhibitor of phospholipase A2. 2 Metabolism of prostaglandin F2alpha by uterine homogenates was undetectable; this was not affected by PBPAB. 3 There was no significant difference between the amounts of arachidonic acid released from uterine homogenates on days 7 and 1k of the oestrous cycle. Small amounts of dihomo-gamma-linolenic acid were detected in the homogenates. 4 The release of arachidonic acid from uterine homogenates was greatly inhibited by PBPAB. 5 Addition of exogenous arachidonic acid to uterine homogenates did not overcome the inhibition of uterine prostaglandin F2alpha synthesis produced by PBPAB. 6 It is concluded that PBPAB inhibits both the release of arachidonic acid from the guinea-pig uterus and its subsequent conversion into prostaglandins.

Key concepts: Arachidonic acid, Prostaglandin F2alpha, Prostaglandins F, Guinea pig, Uterus, Endocrinology, Prostaglandin, Internal medicine

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EFFECT OF p‐BROMOPHENACYL BROMIDE, AN INHIBITOR OF PHOSPHOLIPASE A2, ON ARACHIDONIC ACID RELEASE AND PROSTAGLANDIN SYNTHESIS BY THE GUINEA‐PIG UTERUS in vitro — Research Paper | ScholarLens