Adult rats were made unilaterally cryptorchid (UCD) and 6–7 weeks later Leydig cells were isolated from the scrotal and abdominal testes and their capacity to secrete testosterone in vitro was compared. Basal testosterone production by Leydig cells from the abdominal testes of UCD rats was lowered, compared with cells from the contralateral scrotal testes, whilst their responsiveness to both human chorionic gonadotrophin and an LH releasing hormone agonist was enhanced two- to threefold (P< 0·001) compared both with cells from the contralateral scrotal testes and with cells isolated from untreated rats of the same age. In the UCD rats, concentrations of testosterone in testicular interstitial fluid (IF) were reduced (P< 0·001) by 70–90% in abdominal, compared with scrotal, testes. A similar reduction was evident in the levels of testosterone in spermatic venous blood, and both this decrease and that in IF levels of testosterone varied according to the degree of testicular involution.
The ontogeny of the above changes was investigated. After induction of unilateral cryptorchidism, the weight of the abdominal compared with the scrotal testis declined slowly, such that by day 5 there was only a 25% reduction in weight compared with a 70% reduction by day 40. In contrast, the levels of testosterone in IF from abdominal testes declined rapidly, such that by day 5 an 80% reduction was attained, compared with scrotal testes, with little further change by day 40. Hormone-stimulated testosterone production by Leydig cells isolated from the abdominal testes was unchanged or marginally reduced over the first 3 days compared with cells from the scrotal testes, but by day 5 there was a significant increase in responsiveness; this increase was of smaller magnitude than that evident at day 40. These results suggest a possible association between the fall in intratesticular levels of testosterone induced by unilateral cryptorchidism and the Leydig cell hypertrophy and hyper-responsiveness that occurs in the same testes. The implications with respect to altered Sertoli–Leydig cell interaction are discussed.
J. Endocr. (1984) 102, 319–327
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