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Department of Urology, Showa University School of Medicine, (H.I., H.T., M.W., N.F., H.Y., K.I.) Hatanodai, Shinagawa-ku
The Department of Urology, Faculty of Medicine, University of Tokyo (S.M., M.S., K.F., Y.A.) Kongo, Bunkyo-ku, Tokyo, Japan
The Department of Anatomy, Monash University (D.M.d.K.) Clayton, Victoria, Australia
Address all correspondence and requests for reprints to: H. Ishida, Department of Urology, Showa University School of Medicine, Hatanodai 1-5-8, Shinagawa-ku, Tokyo 142, Japan.
We measured serum inhibin levels in eight untreated patients with prostatic cancer undergoing castration by RIA using an antiserum against 31-kDa bovine follicular fluid inhibin. The inhibin concentrations in testicular tissue and spermatic venous blood were also measured in six of these patients. Serum inhibin levels (mean ± SD, 377.8 ± 212.1 U/L), declined rapidly after castration (15 min after, 233 ± 171.4; 30 min, 224.6 ± 156.6; 1 h, 181.5 ± 95.9; 2 h, 174.3 ± 69.4; 4 h, 122 ± 6.4; 6 h, <120). High concentrations of inhibin were detected n i testicular tissue (31,360 ± 15,180 U/kg), and the levels in spermatic venous blood (3,178.3 ± 1,386.8 U/L) were approximately 10 times greater than those in peripheral blood (385.5 ± 233.1 U/L). Testosterone levels were 1,968.2 ± 992.3 nmol/kg in testicular tissue and approximately 100 times greater in spermatic venous blood (1,631.6 ± 389.7 nmol/L) than in peripheral blood (18.0 ± 4.4 nmol/L). These results suggest that circulating inhibin in men mainly originates from testis and that one of the routes of secretion is via the bloodstream.
Received June 13, 1989.
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