Arachidonic acid metabolism and prolactin secretion in vitro: a possible role for the lipoxygenase products

Neuroendocrinology
P L CanonicoR M MacLeod

Abstract

This study was designed to investigate basal and thyrotropin-releasing hormone (TRH)-stimulated prolactin release in the presence of agents that influence arachidonic acid metabolism. Agents that decrease its production by blocking phospholipase A2 activity, i.e., quinacrine and 4-bromophenacylbromide, significantly decreased prolactin secretion from anterior pituitary glands in vitro and from dispersed pituitary cells in a perifusion column. Phospholipase A2 and phorbol myristate acetate, substances that increase intracellular concentrations of arachidonic acid, markedly stimulated prolactin release by dispersed pituitary cells and by anterior pituitary glands incubated in vitro. The involvement in prolactin secretion of arachidonic acid metabolic products produced via the lipoxygenase pathway was investigated indirectly using nordihydroguaiaretic acid (NDGA), a specific inhibitor of this enzyme. NDGA progressively (dose-related) inhibited the release of prolactin in vitro and blocked the stimulating effect of 50 nM TRH on prolactin release from hemipituitary glands. Indomethacin, a specific inhibitor of the cycloxygenase pathway, had no significant effect on basal and TRH-stimulated prolactin release. The results suggest that...Continue Reading

Citations

Feb 10, 1984·European Journal of Pharmacology·P L CanonicoR M MacLeod
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Dec 1, 1992·Toxicon : Official Journal of the International Society on Toxinology·A M JuddR M MacLeod
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Jul 1, 1984·Molecular and Cellular Endocrinology·A M JuddR M MacLeod
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Jun 1, 1989·Prostaglandins, Leukotrienes, and Essential Fatty Acids·A M Cowell, J C Buckingham
Jun 1, 1985·Proceedings of the National Academy of Sciences of the United States of America·A L HultingB Samuelsson
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Jun 1, 1989·Gynecological Endocrinology : the Official Journal of the International Society of Gynecological Endocrinology·P L Canonico
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