Mature male Sprague-Dawley rats were divided into two groups. One group was rendered bilaterally cryptorchid and the other served as intact controls. Seven, 14, 21, and 28 days post surgery, five animals from each group were sacrificed, blood samples were collected, and the levels of serum gonadotropins and steroids were subsequently determined by RIA. The testes were removed and used to determine zero time concentrations of testosterone (T), T production in vitro, the zero time concentrations of 17β-estradiol (E2), and the levels of cytoplasmic estrogen receptor (E2R). LH levels in the cryptorchid group increased significantly over the controls at 7 days and remained elevated through 28 days; a similar increase in FSH levels was also detected. Cryptorchidism produced no appreciable effects on the serum steroid levels. No significant difference was detected in the levels of T between the cryptorchid and control groups, and no significant difference in serum E2 levels was detected between the two groups through 21 days; however, a slight but significant decrease in E2 below the control level was observed in the cryptorchid group at 28 days. The concentrations of T in the testis remained relatively constant in the controls, while the levels in the cryptorchid animals increased significantly above controls at 14 days and remained significantly elevated through 28 days. A similar increase above controls in the 3-h T production in vitro was found to be significant at 14 days (P < 0.05) and 28 days (P < 0.01). The levels of testicular E2 remained relatively unchanged up to 28 days, at which time the E2 levels were significantly reduced below control levels. However, when the data were expressed as content per testis, the levels of both steroids and T production in the cryptorchid group were found to be reduced compared to control levels. The demonstration that bilateral cryptorchidism resulted in a decreased production of testicular steroids suggests damage to or loss of Leydig cells. The cytoplasmic E2R-binding capacity, expressed as femtomoles of E2 per mg cytosol protein, was found to be increased 2- to 4-fold over that of the control group; this increase was detectable as early as 7 days post surgery. Thus, concomitant to the reduced steroid production, the E2R-binding capacity, which is localized in the Leydig cell, was dramatically increased. This indicates that Leydig cell responsiveness, as reflected by androgen production, was impaired by cryptorchidism. The adverse effects of cryptorchidism, however, did not extend to all functions of the Leydig cell, since E2R binding was enhanced. The demonstration that serum gonadotropins increased while serum steroids remained unchanged after cryptorchidism suggests the possibility that testicular factors other than T and E2 might be involved in the feedback control of the hypothalamic-pituitary axis.