Effects of C₂₁Steroids on Sex Accessory Organs and Testes of Mature Hypophysectomized Rats¹

Abstract

Adult hypophysectomized male rats were treated with 2 mg/day of testosterone propionate, pregnenolone, 17alpha-hydroxypregnenolone, progesterone or 17alpha-hydroxyprogesterone. The treatment commenced on the day of surgery and was continued for 4 weeks. In all steroid treated animals, spermatogenesis was qualitatively maintained. Sex accessory organs were maintained only in testosterone propionate treated animals. In C21 steroid-treated rats the sex accessory organs showed atrophy similar to untreated hypophysectomized animals suggesting lack of peripheral conversion to androgens. However, administration of 3H-pregnenolone with the last injection of pregnenolone resulted in the isolation of a considerable amount of 3H-testosterone from testicular tissue of the experimental animals. This finding suggests that maintenance of spermatogenesis in pregnenolone treated animals could have been due to testosterone formed in the testes from the exogenously administered pregnenolone.

A quantitative assessment of the gametogenic and androgenic properties of testicular steroids in hypophysectomized rats

“…In confirmation of previous observations (Harris & Bartke, 1975;Steinberger et al, 1975) there appeared to be little peripheral formation of androgens as evidenced by the atrophie condition of the accessory sex organs and the low circulating concentrations of testosterone in animals receiving C21 steroids (Table 2). The administration of C21 steroids increases the concentration of testosterone in the rete testis fluid (Harris & Bartke, 1975) and testicular tissue (Parvinen, Hurme & Niemi, 1970;Steinberger et al, 1975), suggesting that these precursors may be metabolized to testosterone within the testis. In intact animals the Leydig cells are the principal site of circulating androgens and significant amounts of testosterone may be channelled directly from the interstitium to the seminiferous tubules (Müller, 1957;Fawcett, Heidger & Leak, 1969).…”

“…The steroids 20a-dihydroprogesterone and 3ß-hydroxy-5a-pregnan-20-one exhibited no gametogenic activity and very weak androgenic potency (Tables 1, 2 and 3). The gametogenic properties of C2i steroids which are intermediates in testosterone biosynthesis but have low intrin¬ sic androgenic activity have been attributed to their bioconversion to androgens (Harris & Bartke, 1975;Steinberger et al, 1975). The site of this conversion is unresolved.…”

“…However, it has been suggested that the seminiferous tubules of hypophysectomized rats, when provided with precursor steroids, may be able to provide sufficient local concentrations of androgens for spermatogenesis (Harris & Bartke, 1975). The concept of intratesticular conversion of exogenous steroids to androgens was developed to explain the approximately equivalent or inferior effects of C21 steroids when com¬ pared to testosterone propionate (Harris & Bartke, 1975;Steinberger et al, 1975). This hypothesis requires qualification to explain the present demonstration of the superior gametogenic effects of progesterone as compared to testosterone.…”

“…The ability of testosterone to maintain spermato¬ genesis has been extensively investigated (see Steinberger, 1971, for review). The possible role of other steroids which characterize the pattern of steroid metabolism in the seminiferous tubules has received little attention although it is known that C21 steroids may possess gametogenic properties (Harris & Bartke, 1975; Steinberger, Chowdhury, Tcholakian & Roll, 1975). The present work evaluates the ability of progesterone, 20a-dihydroprogesterone and 3ß-hydroxy-5a-pregnan-20-one to maintain the quantitative aspects of spermatogenesis with reference to their androgenic potency.…”

Dependence of Testicular Germ Cells on Hormones: A Quantitative Study in Hypophysectomized Testosterone-Treated Rats

“…On day 29 and thereafter a relative steady-state is reached, and germ cell number undergoes no further drastic reduction. Several investiga¬ tors have demonstrated that changes in the testes after hypophysectomy can be prevented and qualitative spermatogenesis can be maintained in rats by C19 or C21 steroids (Nelson & Gallagher, 1936;Selye & Friedman, 1941;Masson, 1945;Steinberger, Chowdhury, Tcholakian & Roll, 1975). Utilizing quantitative techniques Clermont & Harvey (1967) showed that maintenance of spermatogenesis in testosteronetreated hypophysectomized rats is qualitative in nature since a 30-40% reduction in the number of type A spermatogonia was detected in the testosterone-replaced animals.…”