Hemicastration Causes and Testosterone Prevents Enhanced Uptake of [3H] Thymidine by Sertoli Cells in Testes of Immature Rats 1

Abstract

Rat pups were hemicastrated and uptake of [3H] thymidine by Sertoli cells in the remaining testis was compared to that in testes of sham-operated pups at intervals of from 8 h to 21 days after surgery. Labeled thymidine was administered subcutaneously 2 h before sacrifice. Testes were processed for light microscope autoradiography and the percent of Sertoli cell nuclei that had incorporated [3H] thymidine was determined by scoring nuclei in tissue sections as labeled or unlabeled. The percentage of cells labeled was increased in hemicastrates over intact controls by 8 h after surgery and testicular hypertrophy became apparent in hemicastrates by the following day. Labeling of Sertoli cells in hemicastrates remained elevated for 4 days and then returned to normal. When plasma levels of gonadotropins were measured in both groups 4 days after surgery, follicle-stimulating hormone (FSH) was found to be more than twice normal in hemicastrates while luteinizing hormone (LH) was unchanged. The effect of testosterone on the response of Sertoli cells to hemicastration was also examined. In hemicastrates, 2 days of androgen therapy depressed, and an additional 2 days abolished, the proliferative response of the Sertoli cells. Our findings suggest that increased proliferation of Sertoli cells within the remaining testis is involved in the enlargement of the testis that follows hemicastration. They also imply that prevention of compensatory hypertrophy by testosterone involves interference with this response of Sertoli cells in some way. Finally, our data implicate FSH in control of Sertoli cell proliferation in vivo in immature rats.

Development of the seminiferous tubules after neonatal hemicastration in the boar

“…However, since seminiferous tubule diameter did not change, and proliferation of Sertoli cell numbers has been reported previously after hemicastration in boars and several other species (Jenkins & Waites, 1983;Waites et al, 1983;Orth et al, 1984;Hochereau de Reviers et ai, 1984;Putra & Blackshaw, 1985), the compensatory increase in mass of Sertoli cells observed here is probably due to proli¬ feration of Sertoli cell numbers.…”

“…Immature Sertoli cells of several species show increased mitotic activity in response to FSH (Courot, 1967;Steinberger & Steinberger, 1977;Fritz, 1978;Chevalier, 1979;Means et ai, 1980) and may be involved in compensatory Sertoli cell proliferation in neonatally hemicastrated rams and rats (Waites et ai, 1983;Orth et al, 1984). FSH in Group-HC boars was elevated above values for intact animals only during the last 14 days of compensatory Sertoli cell proliferation, whereas plasma GH concentration in Group-HC boars was elevated during the entire period of compensatory proliferation of Sertoli cells (Kosco et ai, 1987 Staining 1 % toluidine blue; 400.…”

The Sertoli Cell – A Hormonal Target and ‘Super’ Nurse for Germ Cells That Determines Testicular Size

“…This is the only cell type in the testis that expresses receptors for this hormone, which, in combination with other factors [12, 13], is well established to be required for adequate Sertoli cell proliferation [14, 15]. Moreover, FSH stimulates the aromatase activity and production of, e.g., inhibin, lactate, transferrin and AR by Sertoli cells [16,17,18,19].…”

Application of morphometric techniques to postnatal rat testes in organ culture: insights into testis growth

“…No significant changes were recorded in Sertoli cell number per cord cross section or in the diameter of the Postnatal treatment of rats with FSH (Meacham et al 1996) as well as postnatal hemicastration, which elevates endogenous FSH levels (Cunningham et al 1978;Orth et al 1984), result in an increase in adult testis size. Similarly, experimentally induced hypothyroidism leads to an increase in adult testis size (Cooke and Meisami 1991;van Haster et al 1992) associated with an increase in Sertoli cell numbers, implicating thyroid-stimulating hormone (TSH) as a mediator of Sertoli cell division.…”