Dihydrotestosterone-binding protein in cytosols of normal and hypertrophic human prostates, and influence of estrogens and anti-androgens on the binding.

Shimazaki, Jun; Kodama, Takaomi; Wakisaka, Masami; Katayama, Takashi

doi:10.1507/endocrj1954.24.9

Cited by 7 publications

(3 citation statements)

References 14 publications

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“…In our previous report, it was shown that the maximum binding sites for dihydrotes tosterone in cytosols of the normal prostate exceeded those of benign prostatic hypertro phy [10], and the present results confirmed the previous observation, though the mecha nism of increase of binding in the normal prostate is obscure.…”

Section: Discussionsupporting

confidence: 92%

Binding of Dihydrotestosterone, R 1881 and R 5020 in Cytosols from Normal, Benign Hypertrophic and Cancerous Human Prostates

Nozumi¹,

Sato²,

Itô³

et al. 1981

Urol Int

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The binding of dihydrotestosterone, R 1881 and R 5020 as examined in cytosols of normal, benign hypertrophic and cancerous tissues of the human prostates. Almost all samples obtained by open operation showed high affinity binding to these ligands. Dissociation constants of the binding to these ligands were approximately 10^––9M irrespective of the pathological state of the prostates. Maximum binding sites for dihydrotestosterone seemed to be greater in normal tissues than in the pathological ones. However, maximum binding sites for R 1881 and R 5020 were not significantly different among the normal and pathological prostates examined in the present study. Moreover, some correlation was observed between the maximum binding sites for R 1881 and those for R 5020. The samples resected by TUR seemed to be inadequate for analyses of androgen binding.

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Section: Discussionsupporting

confidence: 92%

Binding of Dihydrotestosterone, R 1881 and R 5020 in Cytosols from Normal, Benign Hypertrophic and Cancerous Human Prostates

Nozumi¹,

Sato²,

Itô³

et al. 1981

Urol Int

Self Cite

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“…Estrogens may inhibit androgen-sensitive male accessory sex organs indirectly through the lowering of plasma androgen levels due to effects of gonadotrophin secretion and testicular androgen biosynthesis (Price and Williams-Ashman, 1961;Samuels et al, 1964;Oshima et al, 1967;Perklev and Groning, 1969) or alternately, through direct affects on androgen-sensitive glands such as direct in-hibition of the prostate in hypophysectomized dog (Goodwin et al, 1961). Estrogens also cause a decrease in a variety of metabolic processes in target organs, but conversely cause a n increase in prostatic lysosomal activity (Lasnitzki et al, 1965;Mangan et al, 1967;Maggi et al, 1970;Leav et al, 1971;Yamanaka et al, 1975 a,b;Shimazaki et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

Development of seminal vesicles and coagulating glands in neonatal mice. I. The morphogenetic effects of various hormonal conditions

Lung

Cunha

1981

Anat. Rec.

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Seminal vesicles (SV) and coagulating glands (CG) from neonatal mice 1- to 7-days old were observed in whole mount preparations. Untreated, normal SV developed elaborate epithelial branches beginning on day 3 with secondary branches appearing on day 6. Castration (C), estradiol treatment (E), and castration combined with estradiol treatment (C + E) inhibited the morphogenesis of the epithelial branches. Untreated CG formed solid epithelial stalks that developed lateral epithelial buds on day 3 which attained a complex morphological pattern by day 7. Treatment groups (C, E and C + E) displayed a pattern of retarded growth with few epithelial buds appearing even at day 7. The effects of castration on both SV and CG were reversed by the addition of testosterone. Short term in vitro culture of 1-day-old SV and CG glands in control medium or medium supplemented with estradiol did not exhibit visible growth. Culture of SV and CG glands with testosterone or a piece of testis showed pronounced development.

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“…February1979 metabolites of this compound for the intracellular 5a-dihydrotestosterone receptor (Varkarakis et al, 1975;Shimazaki et al, 1977). AA560is also a derivative of anilide and its antiandrogenic action was reported to be about three times as strong as SCH13521 (Takahashi et al, 1977).…”

Section: Endocrinolmentioning

confidence: 99%

Effects of antiprostatic agents on 5.ALPHA.-dihydrotestosterone binding to rat hypophyseal and hypothalamic cytosol macromolecules.

et al. 1979

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Dihydrotestosterone-binding protein in cytosols of normal and hypertrophic human prostates, and influence of estrogens and anti-androgens on the binding.

Cited by 7 publications

References 14 publications

Binding of Dihydrotestosterone, R 1881 and R 5020 in Cytosols from Normal, Benign Hypertrophic and Cancerous Human Prostates

Binding of Dihydrotestosterone, R 1881 and R 5020 in Cytosols from Normal, Benign Hypertrophic and Cancerous Human Prostates

Development of seminal vesicles and coagulating glands in neonatal mice. I. The morphogenetic effects of various hormonal conditions

Effects of antiprostatic agents on 5.ALPHA.-dihydrotestosterone binding to rat hypophyseal and hypothalamic cytosol macromolecules.

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