Inhibitory effect of arachidonic acid on the synthesis of prolactin in human decidual tissues
Kinoshita, T.; Taketani, Y.; Mizuno, M.
Nihon Sanka Fujinka Gakkai Zasshi 42(12): 1607-1612
1990
ISSN/ISBN: 0300-9165 PMID: 2126023 Document Number: 367371
Much evidence indicates that human tissues produce prolactin. However, little is known as to which agents regulate its production in decidual tissues. Therefore, it is of interest to examine the effect of arachidonic acid on the production of prolactin, since it is present in considerably large amounts in decidual tissues. The addition of arachidonic acid to culture media resulted in a significant reduction in the amount of prolactin secreted from incubated decidual tissues in a dose-related fashion. Other poly-unsaturated fatty acids, i.e. linoleic and .gamma.-linolenic acid also inhibited its secretion, whereas saturated fatty acid and mono-unsaturated fatty acids, such as oleic acid, were without effect. The addition of phospholipase A2 and phospholipase C, enzymes to liberate arachidonic acid from phospholipids, also suppressed the secretion of prolactin. Indomethacin and BW-755C, inhibitors of cyclooxygenase and lipoxygenase, respectively, had essentially no effect on the secretion of prolactin. Translatable mRNA for prolactin was detected in decidual tissues. Arachidonic acid did not alter either the amount of mRNA in prolactin of the amount of its mRNA as a percentage of total mRNA. Thus, it appears that arachidonic acid possibly plays a role as a physiological regulator of prolactin secretion in human decidual tissues. The action of arachidonic acid is not mediated by cyclooxygenase or lipoxygenase products, suggesting that arachidonic acid itself, or its metabolites other than prostaglandin and leucotriene, may be involved in the regulation of prolactin secretion.