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Last Updated: 2 years ago

Possible Interaction: Arachidonic Acid and Estradiol

Research Papers that Mention the Interaction

This response to estradiol was clearly dose-dependent, and it was further enhanced by addition of arachidonic acid , the precursor for prostaglandin synthesis, to the medium.
Acta endocrinologica  •  1991  |  View Paper
In this study, treatment of steroid-starved ERα-positive MCF-7 and T47D mammary carcinoma cells with 17β-estradiol resulted in increased cellular uptake of the PUFA arachidonic acid ( AA ) and eicosapentaenoic acid (EPA), important building blocks for cellular membranes, and increased ACSL4 protein levels.
Carcinogenesis  •  2017  |  View Paper
Treatment of macrophages with 17-β estradiol elicited an increased arachidonic acid (AA) release and an up-regulation of both cyclooxygenesis-1 and cyclooxygenasis-2 enzymes at both the transcript and protein levels.
Molecular and Cellular Biochemistry  •  2004  |  View Paper
beta-estradiol at 2 different concentrations (10(-…) in the presence of arachidonic acid for various times (5 min up to 24 h) effected an increase in the production of PGI2 (measured … F1 alpha) of 36-47% in the artery and 16-21% in the vein over basal values (100%).
Zentralblatt fur Gynakologie  •  1992  |  View Paper
Arachidonic acid release was increased in the presence of oestradiol sulphate , oestrone and oestradiol but reduced by oestrone sulphate, dehydroepiandrosterone sulphate, progesterone, dehydroepiandrosterone and, to a lesser extent, by pregnenolone sulphate and testosterone sulphate.
The Journal of endocrinology  •  1988  |  View Paper
Pretreatment with 17 beta-estradiol stimulated the LH responses to LHRH, TPA, and low concentrations of AA.
The American journal of physiology  •  1988  |  View Paper
The present findings suggest that oestradiol , at a relatively high concentration, may interfere with the access of arachidonic acid to the cyclo-oxygenase enzyme.
Prostaglandins  •  1987  |  View Paper
We report that arachidonic acid can reverse the inhibition of masculine development in male embryos produced by estradiol-17 beta or by cyproterone acetate, an androgen receptor-site blocker, and that such reversal can be prevented by an inhibitor of cyclooxygenase, such as indomethacin.
Proceedings of the National Academy of Sciences of the United States of America  •  1986  |  View Paper
In the thrombocytes, 17β-estradiol decreased aggregatory response to arachidonic acid and synthesis of thromboxane B2.
Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine  •  1981  |  View Paper