[Interference of testosterone synthesis through HPGA and ERalpha pathway after 17beta-estradiol exposure to regulate spermatogenesis].
Λέξεις-κλειδιά
Αφηρημένη
OBJECTIVE
To evaluate the effects of 17beta-estradiol (E2) exposure on male reproductive endocrine system, and study the potential mechanism.
METHODS
Male Wistar rats were gavaged with E2 (1.00, 0.50, 0.10, 0.01 mg.kg(-1).d(-1)) for 8 weeks, with corn oil as control. The testes weight and testicular organ coefficient and sperm parameter were examined. Serum levels of zinc and calcium were measured by atomic absorption spectrophotometry. Serum hormone concentrations were determined by RIA. The expression of testosterone synthetase mRNA were assessed by RT-PCR. The expression of estrogen and androgen receptor protein were detected by Western blot.
RESULTS
Testis weight and testicular coefficient were significantly declined. Serum testosterone levels were significantly decreased. Serum estradiol levels showed a significant increase in a dose-related manner (P<0.01). Blood zinc had a significant decrease at 0.50 and 1.00 mg.kg(-1) d(-1) (P<0.01). Epididymal cauda sperm counts declined at 0.50 and 1.00 mg/kg (P<0.01). The expression of steroidogenic acute regulatory protein (StAR) and cytochrome cholesterol side-chain cleavage enzyme (P450scc) mRNA were decreased. The expression of ERa protein was increased, and AR protein was decreased.
CONCLUSIONS
Exposure to E2 in puberty could interfere with the development of testis, The potential including testosterone biosynthesis and spermatogensis in adulthood. mechanism may be indirectly through disturbing the balance of HPGA, and directly through up-regulating the level of ERa protein consequently inhibiting testosterone synthetase. Blood zinc was involved in mediating spermatogensis by E2 exposure.
