RESUMO
Leydig cells were isolated from testes of normal, cryptorchid and induced- varicocele rats. These cells were counted and coincubated with and without human Chorionic Gonadotropin (hCG) during 3 hours; thereafter, steroids were measured in the incubation media. Cryptorchid animals showed the lowest number of Leydig cells, the highest Progesterone response to hCG, a slight increment of testosterone and a decrease of estradiol. On the contrary, both left and right testes from varicocele induced rats showed a higher cell number (per g of tissue), lower progesterone response, slightly higher response testosterone and lower testosterone response. These results demonstrate that these conditions of testicular hyperthermia do not affect the number and function of Leydig cells to the same degree. This may be due to differences in the testicular temperature reached with each procedure.
Assuntos
Criptorquidismo/fisiopatologia , Células Intersticiais do Testículo/metabolismo , Varicocele/fisiopatologia , Animais , Temperatura Corporal , Contagem de Células , Células Cultivadas , Gonadotropina Coriônica/farmacologia , Estradiol/metabolismo , Células Intersticiais do Testículo/efeitos dos fármacos , Masculino , Progesterona/metabolismo , Ratos , Ratos Wistar , Testículo/patologia , Testosterona/metabolismo , Testosterona/farmacologiaRESUMO
In the present investigation the function of the Leydig cells, as the response of gonadal steroids to the injections i.m. of 2000 UI of hCG, was studied in 11 normal men, before and after the induction of hyper or hypoprolactinemia with sulpiride and bromocriptine treatments respectively. The normal response to hCG, showed an increment of serum estradiol concentration 24 h and another of serum testosterone 72 h after the administration of the gonadotropin. The serum FSH concentration decreased during the test. An increase of serum LH levels was observed in the hypoprolactinemic state, but the increment of estradiol was lower after injection of hCG. On the other hand, the hyperprolactinemia induced a low basal level of testosterone with a higher response of this steroid to hCG. The results suggest that hyperprolactinemia interfers the estradiol synthesis by Leydig cells while the loss of the trophic effect of prolactin on gonadal steroidogenesis, as seen in hypoprolactinemia produces a decrease of basal testosterone levels without any alteration of the response of this steroid to hCG. We conclude that prolactin plays an important role in the steroidogenesis of Leydig cells in normal men.