Previous data in the literature suggested that narrow and clear cells (also called apical mitochondria-rich cells) were under the control of estrogens and not androgens. Another study showed that lumenal acidification in the rat epididymis is under androgen control. The current study was, therefore, designed to test whether neonatal manipulation of sex steroid levels affected the development of ep-ididymal H+-ATPase-rich cells.
Our data suggest that administration of estrogen (DES or EE), GnRHa, or flutamide can suppress the postnatal development of H+-ATPase-rich cells. We also observed a significant reduction in testis weights and in plasma testosterone levels in all treatment groups, except for animals treated with flutamide (DES + TE was not assessed for plasma testosterone levels). These treatments (GnRHa, DES, EE, and DES + tE) probably retarded testicular growth via suppression of the hypothalamo-pituitary axis and subsequent suppression of gonadotropin secretion, because we have shown that all of these treatments significantly reduce FSH levels and unpublished data). This is supported by the similarity in the degree of testis weight reduction observed between GnRHa and DES/ EE treatments, as has also been reported in other studies, and by the observation that coadministration of GnRHa and DES has no greater effect on testis weight than either treatment alone (unpublished data).