Metabolism of Progesterone by Rat Testicular Homogenates. IV. Further Studies of Testosterone Formation in Immature Testis<i>in Vitro</i>1

Coffey, James C.; French, Frank S.; Nayfeh, Shihadeh N.

doi:10.1210/endo-89-3-865

Cited by 86 publications

(20 citation statements)

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“…1-4) is present in immature rat testes (Inano et al, 1967 ;Coffey et al, 1971 ;Ficher and Steinberger, 1971 ;Yamada et al, 1976), and is present weakly in immature mouse testes (Tsujimura and Matsumoto, 1974), but is absent in immature monkey and human testes (Mizutani et al, 1977). The previous findings and the present results seem to suggest that testes and ovaries show similar prepubertal 5«-androgen synthesis in each species and that the formation of a significant quantity of 5«-androgens may be absent in ovaries of immature humans.…”

Section: Introductionsupporting

confidence: 65%

“…On the other hand, testes of immature rats and immature mice yield 5a-reduced C 19 steroids (5a-androgens) such as androsterone and 5a-androstane-3«, 17(3-diol as major products (Inano et al, 1967 ;Coffey et al, 1971 ;Ficher and Steinberger, 1971 ;Tsujimura and Matsumoto, 1974 ;Yamada et al, 1976). We also found by in vitro and in vivo studies that progesterone was converted to these 5a-androgens primarily by a pathway through 5a-reduced C 21 -steroids (C 21 -soc-steroids) in these immature testes (Yamada and Matsumoto, 1974 ;Tsujimura et al,1975 ;Yamada et al, 1976).…”

Section: Introductionmentioning

confidence: 99%

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Maturation of ovarian steroid biosynthetic pathways in puberty and their hormonal control

Matsumoto¹,

Fukuda²,

Terakawa³

et al. 1979

Ann. Biol. anim. Bioch. Biophys.

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Summary. In rats, mice and rhesus monkeys of different ages, radioactive ( 14 C or 3 H) progesterone, 3 H-5a-pregnane-3,20-dione and/or 34 C-testosterone were incubated with ovarian homogenate or directly injected into the ovary. After treatments, radioactive products in the incubation mixture and in the ovary or ovarian vein blood were extracted isolated, measured and identified.All ovaries from rats, mice and monkeys of different ages converted significant amounts of progesterone to 17-hydroxyprogesterone, androstenedione and/or testosterone. Ovaries from immature rats and immature mice synthesized a significant quantity of 5a-reduced C 21 -17-OH-and C 19 -steroids such as 3a, 17oc-dihydroxy-Soc-pregnan-20-one, androsterone and 5a-androstane-3a, 17p-diol, whereas ovaries from suckling and adult rats and mice, and those from monkeys in all ages formed very little or no 5a-reduced C 2i 17-OHand C 19 steroids. These 5a-androgens produced by immature rodent ovaries were shown to be synthesized mainly by a pathway through 5a-reduced C 21 -stéroids, which was regulated by LH but not by FSH or sex steroids.Introduction.

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Section: Introductionsupporting

confidence: 65%

Section: Introductionmentioning

confidence: 99%

Maturation of ovarian steroid biosynthetic pathways in puberty and their hormonal control

Matsumoto¹,

Fukuda²,

Terakawa³

et al. 1979

Ann. Biol. anim. Bioch. Biophys.

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“…Testosterone, androstenedione, and androstanediol were measured by RIA in plasma, in conditioned medium from in vitro LC cultures, and in supernatants of total testicular homogenates (Coffey et al 1971, Cochran et al 1979, 1981. All samples were assayed in duplicate, and each experimental data point consisted of 3-6 samples.…”

Section: Hormone Assaysmentioning

confidence: 99%

Androgen profiles during pubertal Leydig cell development in mice

Arumugam²,

Zhang³

et al. 2010

Reproduction

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Postnatal Leydig cell (LC) development in mice has been assumed empirically to resemble that of rats, which have characteristic hormonal profiles at well-defined maturational stages. To characterize the changes in LC function and gene expression in mice, we examined reproductive hormone expression from birth to 180 days, and quantified in vivo and in vitro production of androgens during sexual maturation. Although the overall plasma androgen and LH profiles from birth through puberty were comparable to that of rats, the timing of developmental changes in androgen production and steroidogenic capacity of isolated LCs differed. In mice, onset of androgen biosynthetic capacity, distinguished by an acute rise in androstenedione and testosterone production and an increased expression of the steroidogenic enzymes, cytochrome P450 cholesterol side-chain cleavage enzyme and 17a-hydroxylase, occurred at day 24 (d24) rather than at d21 as reported in rats. Moreover, in contrast to persistently high testosterone production by pubertal and adult rat LCs, testosterone production was maximal at d45 in mice, and then declined in mature LCs. The murine LCs also respond more robustly to LH stimulation, with a greater increment in LH-stimulated testosterone production. Collectively, these data suggest that the mouse LC lineage has a delayed onset, and that it has an accelerated pace of maturation compared with the rat LC lineage. Across comparable maturational stages, LCs exhibit species-specific developmental changes in enzyme expression and capacity for androgen production. Our results demonstrate distinct differences in LC differentiation between mice and rats, and provide informative data for assessing reproductive phenotypes of recombinant mouse models.

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“…Testosterone, androstenedione, and 5␣-androstane-3␣-17␤-diol (androstanediol) rather than 5␣-androstane-3␤-17␤-diol were measured in conditioned media from in vitro cultures and supernatant of total testicular homogenates (22)(23)(24). All samples were assayed in duplicate.…”

Section: Hormonal Determinationmentioning

confidence: 99%

Pubertal and Adult Leydig Cell Function in Mullerian Inhibiting Substance-Deficient Mice

Arumugam

Baker

et al. 2005

Endocrinology

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Mullerian inhibiting substance (MIS) causes Mullerian duct regression during sexual differentiation and regulates postnatal Leydig cell development. MIS knockout (MIS-KO) mice with targeted deletions of MIS developLeydig cell hyperplasia, but their circulating androgen concentrations are reportedly unaltered. We compared reproductive hormone profiles, androgen biosynthesis, and the expression of key steroidogenic and metabolic enzymes in MIS-KO and wild-type (WT) mice at puberty (36 d) and sexual maturity (60 d). In pubertal animals, basal testosterone and LH concentrations in plasma were lower in MIS-KO than WT mice, whereas human chorionic gonadotropin-stimulated testosterone concentrations were similar. In adults, basal LH, and both basal and human chorionic gonadotropin (hCG)-stimulated testosterone concentrations were similar. Purified Leydig cells from pubertal MIS-KO mice had lower testosterone but higher androstanediol and androstenedione production rates. In contrast, testosterone, androstanediol, and androstenedione production rates were all lower in adult MIS-KO Leydig cells. Steroidogenic acute regulatory protein expression was lower in pubertal MIS-KO mice compared with WT, whereas 17␤-hydroxysteroid dehydrogenase and 5␣-reductase were greater, and P450c17 and P450scc were similar. The expression of steroidogenic acute regulatory protein and 17␤-hydroxysteroid dehydrogenase was lower in adult MIS-KO mice, whereas that of 5␣-reductase, P450c17, and P450scc was similar. MIS not only induces regression of the Mullerian ducts during male sexual differentiation (3-5) but also plays a critical paracrine role in the regulation of Leydig cell development and testosterone biosynthesis (6 -10). MIS has also been shown to inhibit proliferation of prepubertal progenitor Leydig cells and prevent regeneration of Leydig cells after chemical ablation (11,12). These actions of MIS in the testis are mediated directly through the MIS type II receptor, which is abundantly expressed in Leydig cells (7). Male transgenic mice overexpressing MIS have feminized genitalia secondary to fewer Leydig cell numbers and decreased serum testosterone concentrations (4, 13). Conversely, mice with targeted deletions of MIS [MIS knockout (MIS-KO)] and/or its receptor develop Mullerian structures but also manifest Leydig cell hyperplasia, focal Leydig cell tumors, and infertility (14,15). Recently, MIS has been shown to induce FSH mRNA expression and enhance LH␤ promoter activity in a pituitary cell line, indicating that changes in MIS action may also affect the hypothalamic-pituitary-gonadal axis (16).In adult MIS-KO mice, although Leydig cell numbers are increased and the mRNA expression of a key steroidogenic enzyme, P450c17, is more abundant, peripheral testosterone and LH concentrations are reportedly unaffected (8). These observations were surprising in light of the findings of decreased serum testosterone in MIS transgenic mice and the inhibitory actions of MIS on testosterone biosynthesis in both in vitro (6,8,10) and in vivo sy...

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Metabolism of Progesterone by Rat Testicular Homogenates. IV. Further Studies of Testosterone Formation in Immature Testisin Vitro1

Cited by 86 publications

References 0 publications

Maturation of ovarian steroid biosynthetic pathways in puberty and their hormonal control

Maturation of ovarian steroid biosynthetic pathways in puberty and their hormonal control

Androgen profiles during pubertal Leydig cell development in mice

Pubertal and Adult Leydig Cell Function in Mullerian Inhibiting Substance-Deficient Mice

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