Ratnasooriya W D, Sharpe R M
MRC Reproductive Biology Unit, Centre for Reproductive Biology, Edinburgh, U.K.
Int J Androl. 1989 Feb;12(1):44-57. doi: 10.1111/j.1365-2605.1989.tb01284.x.
Rats were treated with a single high dose of methoxy acetic acid (MAA; 650 mg/kg) specifically to deplete seminiferous tubules of pachytene and later spermatocytes. The impact of this selective depletion on subsequent spermatogenesis, sperm output and fertility was then evaluated at intervals ranging from 3 days to 10 weeks. Cauda epididymal sperm number was reduced progressively beyond 2 weeks post-treatment and reached a nadir at 5-6 weeks (28-34% of control values) before recovering progressively back to control levels at 10 weeks. Sperm motility was reduced significantly at 4-7 weeks post-treatment with a nadir at 6 weeks (35% of control values). Thus, at 5-6 weeks after MAA treatment, motile sperm output was reduced by 82-88%. Despite these changes, there was little evidence for infertility in the majority of treated males during a serial mating trial. Evaluation of seminiferous tubule morphology combined with germ cell counts at stage VII of the spermatogenic cycle confirmed that, initially, MAA induced the specific loss of pachytene and later spermatocytes at all stages other than early to mid stage VII. Maturation depletion of germ cells at later intervals was consistent with the initial effects of MAA, although at 21 days post-treatment a number of unpredicted (? secondary) changes in spermatogenesis were observed. These were (a) a reduction in number of pachytene spermatocytes at late stage VII/early stage VIII, (b) retention of sperm at stages IX-XIV, and (c) increased degeneration of pachytene spermatocytes and round spermatids at stage VII and of secondary spermatocytes at stages XIV-I. Whilst none of these changes was severe, together they probably accounted for the unexpectedly prolonged drop in sperm output. It is concluded that whilst deleterious changes in spermatogenesis may occur secondarily following MAA treatment, for the most part spermatogenesis proceeds normally and fertility is largely maintained despite a massive but transient decrease in sperm output.
给大鼠单次高剂量注射甲氧基乙酸（MAA；650毫克/千克），专门用于耗尽粗线期及后期精母细胞的生精小管。然后在3天至10周的时间间隔内评估这种选择性耗尽对后续精子发生、精子输出和生育能力的影响。治疗后2周后，附睾尾部精子数量逐渐减少，在5 - 6周时降至最低点（为对照值的28 - 34%），之后逐渐恢复至10周时的对照水平。治疗后4 - 7周精子活力显著降低，在6周时降至最低点（为对照值的35%）。因此，在MAA治疗后5 - 6周，有活力的精子输出减少了82 - 88%。尽管有这些变化，但在连续交配试验中，大多数接受治疗的雄性大鼠几乎没有不育的证据。对生精小管形态的评估以及生精周期VII期的生殖细胞计数证实，最初，MAA导致除VII期早期至中期外的所有阶段粗线期及后期精母细胞特异性缺失。后期生殖细胞的成熟耗竭与MAA的初始作用一致，尽管在治疗后21天观察到精子发生有一些未预测到的（？继发性）变化。这些变化包括：（a）VII期末/ VIII期初粗线期精母细胞数量减少；（b）IX - XIV期精子滞留；（c）VII期粗线期精母细胞和圆形精子细胞以及XIV - I期次级精母细胞的退化增加。虽然这些变化都不严重，但它们可能共同导致了精子输出意外地长期下降。结论是，虽然MAA治疗后精子发生可能继发有害变化，但在大多数情况下，精子发生仍正常进行，尽管精子输出大量但短暂减少，生育能力在很大程度上得以维持。
