Assessment of the biological potency of an estrogen in the human has been and remains a formidable task. The problem arises not only from the lack of a readily distinguished physiological endpoint, but also from the diversity of the biological actions of the estrogens. Estrogens exert proliferative effects in recognized target tissues such as endometrium, vagina, and breast,1 and this action is the one commonly associated with the term "estrogenicity." Estrogens, however, also participate in inducing a host of other peripheral responses in tissues such as blood, bone, skin, and others.2 More importantly, the estrogens also exercise major regulatory functions in the central nervous system, including control of pituitary hormone secretion3 and influencing behavior such as food intake4 and sexual receptivity.5
Much attention had been devoted to the design of estrogen structures that would exhibit a specific type of estrogenic activity, such as gonadotropic regulation, without retaining any uterotropic action. Despite the vast numbers of structures synthesized, little clear-cut separation of these activities has been achieved, suggesting that these dual actions of estrogens may be inextricably linked to each other. On the other hand, much effort has also gone into the study of the mechanism of estrogen action in the uterus and in the central nervous system; despite much progress in both directions, little evidence of a commonality between these two responses to estradiol has so far emerged, suggesting that they may not be directly linked.
In our studies, we sought to examine whether estradiol metabolism may play a critical role in the expression of the biological activity of the female sex hormone.
- Copyright © 1978 by the American Academy of Pediatrics