Hormone treatment after irradiation stimulates recovery of rat spermatogenesis from surviving spermatogonia.
Hormone treatment after irradiation stimulates recovery of rat spermatogenesis from surviving spermatogonia.
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DOI：
10.1002/j.1939-4640.1997.tb01879.x
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发表时间：
1997-01
影响因子：
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通讯作者：
M. Meistrich;M. Kangasniemi
中科院分区：
文献类型：
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作者：
M. Meistrich;M. Kangasniemi
在LBNF大鼠中测试了使用激素治疗刺激照射后精子发生恢复的可能性。在3.5戈伊照射后10周，未接受激素治疗的大鼠中显示精子发生恢复（再生指数）的小管百分比为37%。促性腺激素释放激素激动剂（GnRH-Ag）与唑雷德联合治疗或持续睾酮治疗均显著促进精子发生的恢复。3.5-戈伊照射后立即开始GnRH-Ag治疗并维持10周，再增殖指数为91%。当在10周GnRH治疗和处死大鼠之间允许额外的6.5周不进行进一步治疗时，再增殖指数恢复到100%，精子计数恢复到83 × 10（6）。这些精子数量比未给予激素治疗的大鼠高出100倍以上，是正常未照射对照水平的50%。GnRH-Ag 10周也刺激了6戈伊照射大鼠的生精恢复，即使治疗开始延迟到照射后18周。在没有GnRH-Ag的情况下，再增殖指数为0，但在GnRH-Ag治疗的大鼠中，再增殖指数为14.5%。由于所有的激素治疗都抑制睾丸内睾酮，高水平的睾酮可能会抑制分化，而它们的抑制可能会刺激恢复。尽管确切的机制尚不清楚，但该方法仍可能适用于临床，以激活因辐射或其他细胞毒性治疗而导致无精子症的患者的精子发生。
The possibility of stimulating the recovery of spermatogenesis after irradiation using hormone treatment was tested in LBNF, rats. At 10 weeks after irradiation with 3.5 Gy, the percentage of tubules showing recovery of spermatogenesis (repopulation index) was 37% in rats that received no hormone treatment. GnRH agonist (GnRH-Ag) treatment with Zoladex or continuous treatment with testosterone markedly stimulated the recovery of spermatogenesis. When GnRH-Ag treatment was started immediately after 3.5-Gy irradiation and maintained for 10 weeks, the repopulation index was 91%. When an additional 6.5 weeks without further treatment was allowed between the 10-week GnRH treatment and killing the rats, the repopulation index recovered to 100% and sperm counts to 83 x 10(6). These sperm counts were more than 100-fold higher than those in rats not given hormone treatment and 50% of normal nonirradiated control levels. GnRH-Ag for 10 weeks also stimulated spermatogenic recovery in rats irradiated with 6 Gy, even when the start of treatment was delayed until 18 weeks after irradiation. Without GnRH-Ag, the repopulation index was 0, but in GnRH-Ag-treated rats it was 14.5%. Since all of the hormone treatments suppress intratesticular testosterone, high levels of testosterone may be inhibiting differentiation and their suppression may stimulate recovery. Even though the exact mechanism is not yet known, this method may still be applicable for clinical use to activate spermatogenesis in patients rendered azoospermic by irradiation or possibly by other cytotoxic treatments.