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.
No takes yet. Share an insight, caveat, or question.
Mitchell et al. (1977) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: