Octylphenol (OP), an environmental estrogen, stimulates prolactin (PRL) gene expression.

A growing concern about "endocrine disrupters" and their impact on estrogen-dependent-phenomena led us to investigate the effects of OP, an environmental estrogen, on PRL gene expression. To this end, we found that OP stimulates the PRL gene to a similar degree as estradiol (E2), although E2 is a 1000-fold more potent in this regard. We then sought to confirm that OP exerts its effects through E2-receptors. Accordingly, we treated cells with tamoxifen (TAM), an anti-estrogen, and found that it blunted the response induced by OP, suggesting that E2-receptors mediated this response. Finally, using "real time" measurements of gene expression in living cells, we found that a large fraction of mammotropes were OP-responsive. These results clearly demonstrate that OP affects PRL gene expression in a manner identical to that of E2. Inasmuch as PRL subserves an obligatory role in the regulation of lactation as well as in neonatal development, we believe that environmental estrogens such as OP have the potential to adversely affect the maternal-infant unit by altering PRL gene expression.