Zhou B, Hutson J M, Hasthorpe S
The F. Douglas Stephens Surgical Research Laboratory, Royal Children's Hospital Research Institute, Melbourne, Australia.
Br J Urol. 1998 Feb;81(2):290-4. doi: 10.1046/j.1464-410x.1998.00513.x.
To determine whether cryptorchidism is a congenital malformation and whether the impaired spermatogenesis in immature testes can be reversed by early orchidopexy, using the mutant trans-scrotal (T-S) rat which is normally masculinized but has cryptorchidism in 85% of males.
First, T-S rats (six per group) with ectopic testes destined to be undescended were investigated histologically at 4, 7 and 14 days after birth. Secondly, 12-day-old T-S rats were divided into four groups which underwent different procedures, i.e. 1, with normally descending testes (normal control, 10 rats); 2, with undescended testes (UDT) treated by orchidopexy (treated UDT, eight rats); 3, with UDT treated by a sham operation (sham-operated UDT, six rats); and 4, with UDT left untreated (untreated UDT, six rats). Thirty days after operation the testicular anatomy was recorded; excised testes were examined histologically and different types of germ cells were counted per tubule cross-section microscopically.
There were no quantitative or morphological differences in the numbers of gonocytes, type-A spermatogonia or Leydig cells in the seminiferous tubules between normal and ectopic testes in the first 14 days after birth. However, by 21 days of age spermatogenesis in the UDT had declined with transformation from primary leptotene spermatocytes to spermatids. There were significantly more Leydig cells in the untreated UDT at 30 days than in normal control testes. The impaired spermatogenesis in UDT was restored by early orchidopexy and there were significantly more seminiferous tubules at stage 3 (pachytene spermatocytes) and stage 4 (spermatids) than in the untreated or sham-operated groups (P < 0.001).
These results show that in the T-S rat with cryptorchidism, the testicular damage is not a congenital malformation and can be reversed with early surgical correction.
利用突变的经阴囊（T-S）大鼠来确定隐睾症是否为先天性畸形，以及未成熟睾丸中受损的精子发生是否能通过早期睾丸固定术得以逆转，该大鼠通常会发生雄性化，但85%的雄性大鼠患有隐睾症。
首先，对出生后4天、7天和14天的异位睾丸注定无法下降的T-S大鼠（每组6只）进行组织学研究。其次，将12日龄的T-S大鼠分为四组，分别进行不同的处理，即1组，睾丸正常下降（正常对照组，10只大鼠）；2组，隐睾经睾丸固定术治疗（治疗后的隐睾组，8只大鼠）；3组，隐睾进行假手术治疗（假手术治疗的隐睾组，6只大鼠）；4组，隐睾不进行治疗（未治疗的隐睾组，6只大鼠）。术后30天记录睾丸解剖结构；切除的睾丸进行组织学检查，并在显微镜下对每个小管横截面上不同类型的生殖细胞进行计数。
出生后前14天，正常睾丸和异位睾丸的生精小管中生殖母细胞、A型精原细胞或睾丸间质细胞的数量在数量或形态上均无差异。然而，到21日龄时，隐睾组的精子发生减少，从初级细线期精母细胞转变为精子细胞。30天时，未治疗的隐睾组的睾丸间质细胞明显多于正常对照组睾丸。早期睾丸固定术可恢复隐睾组受损的精子发生，与未治疗或假手术组相比，第3阶段（粗线期精母细胞）和第4阶段（精子细胞）的生精小管明显更多（P<0.001）。
这些结果表明，在患有隐睾症的T-S大鼠中，睾丸损伤不是先天性畸形，早期手术矫正可使其逆转。
