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Departments of Medicine and Cell Biology, Baylor College of Medicine, Veterans Administration Hospital Houston, Texas 77211
Address requests for reprints to: Glenn R. Cunningham, M.D., Veterans Administration Hospital, 2002 Holcombe Boulevard, Houston, Texas 77211.
Abstract
To determine if high intratesticular concentrations of testosterone are essential for completion of spermatogenesis, intact 90-day-old Charles River CD rats were treated with testosterone propionate (TP). Pilot studies indicated that sc administration of 100 /xg TP/100 g BW-day caused maximum suppression of testicular testosterone. This dose was administered for 13 days and animals were killed 24 h after the last injection. Intrastesticular levels of testosterone were reduced 30- fold from 0.295 ± 0.04 to 0.01 ± 0.001 ng/mg testis, and serum levels of FSH were suppressed 33% from 238 ± 15 to 195 ± 5 ng/ ml (P < 0.001). However, testicular weight only fell from 1.598 ± 0.058 to 1.482 ± 0.026 g, and qualitatively, spermatogenesis was normal.
To examine the possibility that morphological changes failed to occur because the period of treatment was too short, a second group of animals were treated with the same dose of TP for 39 days. Once again, the intratesticular concentration of testosterone was suppressed from 0.196 ± 0.35 to 0.006 ± 0.002 ng/ml testis (P < 0.001) and the serum concentration of FSH was reduced from 298 ± 53 to 205 ± 34 ng/ml (P < 0.05). Testicular weight only fell from 1.660 ± 0.028 to 1.455 ± 0.057 g, and complete spermatogenesis occurred. At this interval, however, a few abnormal and probably dysfunctional Sertoli cells as well as some degenerating pachytene spermatocytes and spermatids were observed. In the testis, the amount of androgen-binding protein fell from 16.34 ± 1.14 to 6.65 ± 0.99 pM/testis (P < 0.001), but it was not significantly altered in the epididymis.
These observations indicate that persistance of complete spermatogenesis in the adult rat is not dependent upon high intratesticular levels of testosterone and suggest that FSH, which is known to regulate Sertoli cell function, may, as a result, secondarily influence germ cell maturation.
Footnotes
* This work was supported by the V.A. (MRIS 0550) and NIH Grant HD-07655.
Received September 11, 1976.
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