Meachem S J, Wreford N G, Stanton P G, Robertson D M, McLachlan R I
Prince Henry's Institute of Medical Research, Monash University, Clayton, Victoria, Australia.
J Androl. 1998 Nov-Dec;19(6):725-35.
The role of follicle-stimulating hormone (FSH) in adult rat spermatogenesis is unclear. Although exogenous testosterone (T) restores spermatogenesis following gonadotropin-releasing hormone (GnRH) immunization or T plus estradiol (TE) treatments, an assessment of the independent action of T and FSH was not possible, as exogenous T treatment maintains serum FSH levels. We have used passive immunization against FSH to determine whether T alone is capable of reinitiating spermatogenesis after chronic and acute FSH withdrawal. Adult rats received T-filled Silastic implants 6 cm (T6) or 8 cm (T24) in length for 7 days in combination with either a polyclonal sheep antisera raised against rat FSH (FSHAb, 2 mg/kg SC daily) or control sheep immunoglobulin (ConAb) after either GnRH immunization (12 weeks) or TE treatment (9 weeks). The neutralizing capacity of the FSHAb was determined using a FSH in vitro bioassay; this analysis demonstrated that administration of FSHAb in vivo reduced FSH levels by >90%. Testes were fixed and germ cell number per testis quantified using the optical dissector. GnRH immunization reduced spermatogonia, pachytene spermatocytes, and round spermatids to 50, 13, and <1% of normal, respectively. T6 and T24 Silastic implants with the inclusion of the FSHAb did not increase the number of spermatogonia, pachytene spermatocytes, and round spermatids (50, 15, and 1% of normal, respectively). T6+ConAb treatment increased spermatogonial, pachytene spermatocyte, and round spermatid numbers to 74, 30, and 3% of normal, respectively (P < 0.05). No further increases were seen with T24 implants. TE treatment suppressed pachytene spermatocytes and round spermatids to 33 and 1% of normal, respectively (P < 0.05). T6+FSHAb treatment did not increase the number of pachytene spermatocytes and round spermatids (36 and 8%, respectively), whereas T6+ConAb treatment increased pachytene spermatocyte and round spermatid number to 50 and 28% of normal, respectively (P < 0.05). T24+FSHAb treatment increased the number of pachytene spermatocyte and round spermatids (56 and 22% of normal, respectively; P < 0.05), whereas T24+ConAb treatment increased these cells forms to 79 and 31% of normal, respectively. In conclusion, T alone is unable to restore spermatogenic cell populations in the setting of chronic FSH withdrawal. Although acute FSH withdrawal markedly impairs the restoration process, higher doses of T can partially compensate for the lack of FSH. These data suggest that FSH is important for the initial phase of spermatogenic restoration.
促卵泡激素（FSH）在成年大鼠精子发生中的作用尚不清楚。尽管外源性睾酮（T）可在促性腺激素释放激素（GnRH）免疫或T加雌二醇（TE）处理后恢复精子发生，但由于外源性T处理可维持血清FSH水平，因此无法评估T和FSH的独立作用。我们使用抗FSH的被动免疫来确定在慢性和急性FSH撤除后T是否能够单独重新启动精子发生。成年大鼠接受长度为6 cm（T6）或8 cm（T24）的含T硅橡胶植入物7天，在GnRH免疫（12周）或TE处理（9周）后，联合使用针对大鼠FSH的多克隆羊抗血清（FSHAb，2 mg/kg皮下注射每日）或对照羊免疫球蛋白（ConAb）。使用FSH体外生物测定法确定FSHAb的中和能力；该分析表明，体内给予FSHAb可使FSH水平降低>90%。将睾丸固定，使用光学分割器对每个睾丸的生殖细胞数量进行定量。GnRH免疫使精原细胞、粗线期精母细胞和圆形精子细胞分别降至正常水平的50%、13%和<1%。包含FSHAb的T6和T24硅橡胶植入物并未增加精原细胞、粗线期精母细胞和圆形精子细胞的数量（分别为正常水平的50%、15%和1%）。T6+ConAb处理使精原细胞、粗线期精母细胞和圆形精子细胞数量分别增加至正常水平的74%、30%和3%（P<0.05）。T24植入物未进一步增加。TE处理使粗线期精母细胞和圆形精子细胞分别降至正常水平的33%和1%（P<0.05）。T6+FSHAb处理未增加粗线期精母细胞和圆形精子细胞的数量（分别为36%和8%），而T6+ConAb处理使粗线期精母细胞和圆形精子细胞数量分别增加至正常水平的50%和28%（P<0.05）。T24+FSHAb处理增加了粗线期精母细胞和圆形精子细胞的数量（分别为正常水平的56%和22%；P<0.05），而T24+ConAb处理使这些细胞形式分别增加至正常水平的79%和31%。总之，在慢性FSH撤除的情况下，单独的T无法恢复生精细胞群体。尽管急性FSH撤除明显损害恢复过程，但更高剂量的T可部分补偿FSH的缺乏。这些数据表明FSH对生精恢复的初始阶段很重要。
