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Prince Henry’s Institute of Medical Research (L.O., R.I.M., D.M.R.), Clayton, 3168 Victoria, Australia; and Department of Urology, Yokahama City University School of Medicine (K.S.), 3–9 Fukuura, Kanazawa-ku, Yokahama, Kanagawa 236, Japan
Address all correspondence and requests for reprints to: Liza O’Donnell, Ph.D., Prince Henry’s Institute of Medical Research, P.O. Box 5152, Clayton, 3168 Victoria, Australia. E-mail: liza.odonnell{at}med.monash.edu.au
Spermiation is the process by which mature sperm are released from the Sertoli cell into the lumen of the seminiferous tubule. Previous studies have shown that FSH and LH/testosterone suppression causes a significant increase in the degeneration of mature elongated spermatids. The purpose of this study was to investigate the extent to which spermiation failure contributes to the overall failure of spermatogenesis during hormone suppression. We used in vivo models to selectively suppress either FSH, by passive immunization, and or testosterone, by administration of SILASTIC brand (Dow Corning) testosterone and estradiol implants to suppress LH and testicular testosterone production. Stereological quantitation of the number of step 17–18 spermatids before spermiation and the number of step 19 spermatids retained within the epithelium after spermiation showed that 2% of spermatids failed to spermiate in control animals, and 11% and 14% of spermatids failed to spermiate after 1 week of FSH inhibition or testosterone suppression, respectively. After 1 week of combined FSH and testosterone withdrawal, 50% of the spermatids in the testis failed to be released. A time course of testosterone suppression showed that after 4–5 weeks over 90% of spermatids failed to spermiate. We conclude that spermiation is highly sensitive to hormone suppression, with T and FSH acting synergistically to support spermiation, and that spermiation inhibition is a potential target for contraception.
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