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Therefore, an AI may be taken such as anastrozole to block the conversion of testosterone into estrogen, since it has been demonstrated to produce both estrogenic and antiestrogenic effects, and since they are well understood in terms of their potential adverse effects on the reproduction and function of the male gonads, and on the reproductive and fertility of the female reproductive organs (see , for an review). Thus far, the proposed mechanisms of action of estrogens in the male reproductive system are summarized in . Specifically, we showed that activation of aromatase by estrogens leads to conversion of nandrolone to nandrolone glucuronide, although the amount of that molecule remains within the normal range [2]. The activity of aromatase is mediated by a series of enzymes, including: estrogen receptor-α, ERX/cAMP reaction, and aromatase complex [2]. These enzymes are activated in vitro by aromatized testosterone and estradiol, but also by various estrogens. Aromatase is activated by testosterone only at concentrations that would be below its free fraction on the surface of human cells. This activation of the aromatase complex is stimulated by the action of aromatized T to aromatizing amino acids and other compounds, which are then transported into the nucleus and stored in a variety of tissues. Aromatase is activated by estrogens but not by estradiol. In addition to the direct actions of estrogens, the estrogen receptor-α mediates most of the estrogenic activity of these substances. Estrogen agonists induce the gene expression of genes encoding estrogen receptors in the mouse, the mammalian testis, and the ovary [2, 3], although estradiol also induces mRNA expression at this time [6]. In a model of ovarian cystogenesis in vitro, estrogen receptor α in ovarian tissues increased expression of both estrogen receptors α and β, as revealed by expression immunoprecipitation (EM). We then evaluated the effect of administration of estradiol or TR-15 on both the number of estrogen receptor α (ERα) and estrogen receptors β (ERβ) mRNA in a number of ovarian tissues from women who had undergone a bilateral hysterectomy. This ERβ was specifically elevated in the ovaries of women with hysterectomy, where the cystosympathetic function was abolished, as evidenced by the absence of pulsatile contractions [7]. The results showed that ERα and ERβ mRNA expression was increased by both TR-15 and estradiol. On the other hand, ERα mRNA Related Article:

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