Farrer J H, Sikka S C, Xie H W, Constantinide D, Rajfer J
Fertil Steril. 1985 Jul;44(1):125-32. doi: 10.1016/s0015-0282(16)48689-9.
In an attempt to determine whether the production and synthesis of testosterone (T) by the testis is impaired by the cryptorchid state, the ability of the cryptorchid rat testis to form T was assessed at various time periods into adulthood after the surgical induction of cryptorchidism in the newborn period. The intratesticular T content of the descended testis rose from 0.3 ng/testis at 14 days of age to 71.2 ng/testis at adulthood (day 56); whereas in the cryptorchid testis, the values were 0.4 ng/testis and 2.0 ng/testis, respectively, at the same ages (P less than 0.001). For determination of the site of inhibition of T biosynthesis in the cryptorchid testis, the enzymatic activities (17 alpha-hydroxylase, 17,20-desmolase, and 17 beta-hydroxysteroid dehydrogenase) in the delta 4T biosynthetic pathway were measured. All these enzyme activities in the cryptorchid testis were inhibited at 56 days of age by about 80% when compared with the descended testis (P less than 0.01). These data suggest that cryptorchidism exerts a deleterious effect on the ability of the Leydig cells to synthesize T and may in part explain the abnormal morphology and resultant infertility seen in patients with cryptorchidism.
为了确定隐睾状态是否会损害睾丸产生和合成睾酮(T)的能力,在新生期手术诱导隐睾后,于成年后的不同时间段评估隐睾大鼠睾丸生成T的能力。下降睾丸的睾丸内T含量从14日龄时的0.3 ng/睾丸升至成年期(第56天)的71.2 ng/睾丸;而在隐睾睾丸中,相同年龄时的值分别为0.4 ng/睾丸和2.0 ng/睾丸(P小于0.001)。为了确定隐睾睾丸中T生物合成的抑制位点,测量了Δ4T生物合成途径中的酶活性(17α-羟化酶、17,20-裂解酶和17β-羟类固醇脱氢酶)。与下降睾丸相比,隐睾睾丸在56日龄时所有这些酶活性均被抑制约80%(P小于0.01)。这些数据表明,隐睾症对睾丸间质细胞合成T的能力产生有害影响,这可能部分解释了隐睾症患者出现的异常形态和由此导致的不育症。