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Estrogen and Antiestrogen Action in Reproductive Tissues and Tumors

1979; Elsevier BV; Linguagem: Inglês

10.1016/b978-0-12-571135-7.50010-2

Benita S. Katzenellenbogen, Hemlata S. Bhakoo, E. Ferguson, Nancy C. Lan, Tochiro Tatee, Ten-lin S. Tsai, John A. Katzenellenbogen,

Enzyme function and inhibition

Publisher Summary This chapter describes the mechanisms by which estrogens and antiestrogens regulate the growth of reproductive tissues and of tumors that develop in reproductive tissues. During the normal development of the rat, uterine growth takes place over a period of several weeks; however, one can induce this growth in a dramatic fashion simply by injecting a dose of estrogen into an immature rat. This hormone-induced uterine growth, which occurs over a period of a few days, involves increases in all metabolic activities and increased water uptake, vascularization, and cell division. After exposure to estrogen, the steroid binds to the cytoplasmic receptor present in the target cell. The cytoplasmic receptor becomes localized in the nucleus, and the nuclear receptor interacts with chromatin in a manner such that a whole series of biochemical and physiological responses are elicited as long as the level of hormone is adequate. Hence, the tissue responds and a part of this response entails the replenishment of cytoplasmic receptor that renews the capacity of the tissue to respond further to hormone. This replenishment of cytoplasmic receptor is believed to occur both by the resynthesis of receptor and by the recycling of some receptor from the nucleus back to the cytoplasmic compartment. When an antiestrogen or a more active metabolite of the antiestrogen enters the target cell, it also binds to the cytoplasmic receptor. The antiestrogen–receptor complex does move into the nucleus and binds to chromatin, but its nuclear interaction must be different because it initiates only some responses. In some tissues, like the chick oviduct, it does not appear to evoke any estrogen-like responses, although the receptor does localize in the nucleus. After antiestrogen, cell division eventually becomes arrested and likewise there is no net increase in receptor content in the tissue.