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Disruption of Tubulobulbar Complex by High Intratesticular Estrogens Leading to Failed Spermiation

Division of Neuroendocrinology (R.D., S.P., R.U., M.G.-S., N.H.B.), Confocal Facility (R.G., S.S.), and Division of Electron Microscopy (S.D.), National Institute for Research in Reproductive Health (Indian Council of Medical Research), Parel, Mumbai 400 012, India

Address all correspondence and requests for reprints to: Nafisa H. Balasinor, Neuroendocrinology Division, National Institute for Research in Reproductive Health, Parel, Mumbai 400 012, India. E-mail: nbalasinor{at}rediffmail.com.

Spermiation is the final phase of spermatogenesis leading to release of mature spermatids into the lumen of the seminiferous tubules. Morphologically, it involves a series of events, namely removal of excess spermatid cytoplasm, removal of ectoplasmic specialization, formation of tubulobulbar complex, and final disengagement of the spermatid from the Sertoli cell. Previous studies in our laboratory have shown that administration of 17β-estradiol at a dose of 100 µg/kg body weight for 10 d resulted in failure of spermiation. This was accompanied by a suppression of FSH and intratesticular testosterone with a concomitant rise in intratesticular 17β-estradiol. The present study was undertaken to determine the cause of failure and subsequently the molecular events in spermiation. Electron microscopic and confocal studies revealed an absence of tubulobulbar complex in step 19 spermatids after estradiol treatment, highlighting the significance of these structures in spermiation. It was further observed that treatment affected the Sertoli cell cytoskeleton and Arp2/3 complex that is critical for de novo polymerization of actin during tubulobulbar complex formation. In conclusion, the present study reports the role of 17β-estradiol in inhibiting the formation of tubulobulbar complex, which could be one of the mechanism by which environmental estrogens influence male fertility.

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