**4. Male accessory glands and hormonal control**

Male accessory sex glands display a consistent pattern of differential sensitivity to androgens and estrogens and that these hormones may exert their action on different cell types within the organ [25]. The development and differentiation of the male reproductive system in the fetus are directed by the fetal testis through the production of testosterone and anti-Müllerian hormone. In the fetal testes, Leydig cells produce testosterone, a steroidal hormone that promotes the growth and differentiation of Wolff's ducts such as epididymis and prostate. At the same time, the Sertoli testicular cells produce the Anti-müllerian hormone (HAM) that causes the regression of the Müllerian ducts. The development of the external sexual organs is generated from the differentiation of the genital tubercle, eminence (protuberance) located in front of the cloaca of the embryo. The secretion of the enzyme 5-α-reductase allows the transformation of testosterone to dihydrotestosterone (DHT), a hormone that differentiates the genital tubercle to the male external sex organs [54]. However, the possible impact of other glucocorticoid hormones has been proposed in experimental animals. Betamethasone has been used for inducing fetal lung maturation. Some studies reported that prenatal treatment with this drug reduced testosterone levels in the male fetus. In adulthood stage of these animals, lower values of FSH and sperm quality were observed; seminal vesicle weight was decreased while testicular and ventral prostate weights were increased. The betamethasone exposure leads to long-term reproductive impairment in male rats. It is important to considerate the implications for humans, considering the use of this glucocorticoid in pregnant women [55].

Other drug that has negative impact on secretion of male accessory glands is atorvastatin because reduce acid phosphatases, NAG and L-carnitine in semen during the therapy, indicating an alteration of prostatic and epididymal functions with reduction of seminal parameters. The mechanism of the effect of atorvastatin on the function of accessory glands is not clear; possibly, the reduction in LDL-cholesterol levels affects the synthesis of testosterone by Leydig cells [56]. Dihydrotestosterone (DHT), estradiol, progesterone and prolactin receptors have been found in prostates of rats. It has been shown in these species that testosterone induces hyperplasia and also has an anti-inflammatory effect on that gland [57].

The effect of prolactin on the prostate was studied in hypophysectomized animals treated with LH and FSH without any supply of exogenous prolactin, the animals showed low weight in prostate and seminal vesicles [58]. Prolactin potentiates the effect of androgens on the prostate and seminal vesicles in rodents, possibly favoring the conversion of testosterone to dihydrotestosterone. Hyperprolactinemia in mice produces structural changes in the cells with the highest amount of androgen receptor in the epididymis and prostate [59]. Studies in castrated rats showed that prolactin stimulates the expression of epididymal and sialic acid alpha glucosidases, independent of androgens [60]. The reduction of glandular markers in the absence of infection could be related to unknown hormonal changes.
