Low-dose ethanol suppresses 17β-estradiol activity in GH4C1 pituitary tumor cells

The interaction of chronic alcohol consumption with estrogen has been recognized in various tissues; however, the potential mechanism has not been clearly defined. In this study, we made the following observations: (a) 0.01% (v/v) ethanol (corresponding to 1.7 mM) significantly elevated estrogen receptor alpha (ER alpha) protein content, stimulated activator protein-1 (AP-1)-dependent ER alpha transcriptional activities, and ultimately enhanced GH4C1 cells growth in vitro and (b) the same concentration of ethanol suppressed the stimulatory effects of 17 beta-estradiol (E2; 10 nM) on both cell growth and cellular PRL accumulate through attenuation of ER alpha actions at both the estrogen response element and the AP-1 site. These observations raise the question as to what extent ethanol influences signal transduction pathways controlled by E2 in experimental medicine and biology.