Abstract
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 (ERalpha) protein content, stimulated activator protein-1 (AP-1)-dependent ERalpha transcriptional activities, and ultimately enhanced GH4C1 cells growth in vitro and (b) the same concentration of ethanol suppressed the stimulatory effects of 17beta-estradiol (E2; 10 nM) on both cell growth and cellular PRL accumulate through attenuation of ERalpha 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.
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