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The morphology and function of the apical mitochondria-rich cells in the mammalian ductus epididymidis epithelium are revised. These cells are similar in all mammalian species studied. Apical mitochondria-rich cells are scarce (1 -5 cells/ 100 principal cells) and are mainly found in the initial epididymal segments. Their morphology varies from slender cells that extend from the basal lamina to the epididymal lumen, to round cells that protrude into the lumen and are not in contact with the basal lamina. Their cytoplasm is more electron-dense than that of principal cells and contains more mitochondria which, in some species, are surrounded by rough endoplasmic reticulum cisternae. The adluminal cytoplasm displays a few short microvilli and contains many acid phosphatase positive vesicles. Apical mitochondria-rich cells differ from the principal cells in some histochemical features such as: (a) different lectin-staining pattern; (b) more intense reaction to the enzymatic activities: carbonic anhydrase, Ca2 + -ATPase, peanut-agglutinin-sialidase, NADP dehydrogenase, succinate dehydrogenase, agalactosidase and P-galactosidase; (c) more intense immunoreaction to several cytokeratin types and to estradiol-related receptor protein; (d) weaker immunoreaction to epithelial membrane antigen and to retinol-binding protein.Although the function of the apical mitochondriarich cells is still unknown, the following possible functions have been suggested: holocrine secretion; cooperation with the principal cells in epididymal reabsorption of testicular fluid; and acidification of epididymal fluid. Experimental results suggest that differentiation and maintenance of apical mitochondria-rich cells are not under androgen control and that these cells are sensitive to estrogen stimulation.

No abstract

Topics of interest were the role of sexual transmission by some parasites, principally T. vaginalis, relationship with subfertility or infertility in the male subject, clinical significance in differential diagnosis with other inflammatory processes, and for some parasites the relationship with opportunistic behavior and immunodeficiency syndromes, including the acquired immunodeficiency syndrome.

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A histometric study of the development of the human epididymis from the fetal period to adulthood has been carried out in males without testicular or related pathology, distributed into the following groups: (I) fetuses (between the 28th and 37th week of pregnancy); (II) newborns (1-30 days of age); (III) infants (2-4 months of age); (IV) infants (5-12 months of age); (V) infants (1-4 years of age); (VI) children (5-14 years [prepubertal]); and (VII) adults (15-60 years of age). For each age group and each epididymal portion (efferent ducts, caput, corpus and cauda epididymidis) the parameters measured were (1) total surface (epithelium + muscular layer + lumen); (2) the surface occupied by the lumen; (3) the surface occupied by the muscular layer; (4) total diameter of the duct; (5) total diameter of the lumen; and (6) the height of the epithelium. The results of the present study revealed that the development of the efferent ducts and ductus epididymidis follows a biphasic pattern. A progressive development occurs from the fetal period to infants 2-4-months of age. However, this development is transient and regresses during infancy (groups IV and V). At childhood (group VI), a definitive development is initiated and completed at puberty (group VII). These changes seem to be related to the androgen-dependence of the epididymis, the different stages of testicular maturation, and the steroidogenic activity of Leydig cells.

No abstract

The distribution of the androgen receptor (AR) in archival human testes was determined immunocytochemically using an affinity-purified peptide-specific rabbit antibody, PG21, and employing a modified biotin-streptavidin-immunoperoxidase method that incorporated a biotin amplification step. In combination with microwave epitope retrieval, the biotin amplification step increased the sensitivity of the immunostaining assay approximately 20-fold. Thus, the useful range at which PG21 rendered a robust, specific immunostaining signal without also increasing nonspecific background was extended dramatically. Broadening the useful range of the PG21 antibody made it possible to resolve the relative amounts of immunopositive AR in different cell types of the human testis. At a high PG21 concentration, for example, all AR-positive cells exhibited a robust immunostaining intensity, but it was not possible to distinguish between nuclei exhibiting either high or moderate immunostaining intensities. In contrast, as the concentration of PG21 was decreased, distinct populations of testicular cells exhibited differential AR immunostaining intensities in their nuclei. AR immunostaining of Sertoli cell nuclei was present at low PG21 concentrations at which no immunostaining of peritubular myoid cells or Leydig cells could be detected. In turn, AR immunostaining of peritubular myoid cells was detected at PG21 concentrations that did not immunostain Leydig cells. Moreover, within the seminiferous epithelium, Sertoli cell nuclear AR staining intensity was less at stages V and VI of the cycle of the seminiferous epithelium than that at stage III, and stage III staining intensity was greater than that at stages I and II. This AR immunostaining pattern in human Sertoli cell nuclei as a function of the cycle of the seminiferous epithelium is reminiscent of the pattern observed in rodent species. Finally, no AR immunostaining of germ cells was observed at any of the PG21 concentrations examined.