Aspects of Androgen-Dependent Events as Studied by Antiandrogens

Neumann, F.; Vo, Berswordt-Wallrabe R; Elger, W.; Steinbeck, H.; Jd, Hahn; Kramer, Michael D.

doi:10.1016/b978-0-12-571126-5.50013-3

Cited by 136 publications

(90 citation statements)

References 68 publications

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“…When they are administered to a pregnant mother while her fetus' brain is being sexually organized, offspring are likely to have their postpubertal sexual behavior affected. The best documented effect is the tendency for various antiandrogens to have F/dM effects on the sexual behavior of male rats after the onset of puberty (e.g., presenting and elevating the rear to other males accompanying a failure to mount females; Neumann et al, 1970;Ward, 1972a).…”

Section: Blocking or Augmenting The Effects Ofandrogens With Drugsmentioning

confidence: 99%

Neurohormonal functioning and sexual orientation: A theory of homosexuality–heterosexuality.

Ellis

Ames²

1987

Psychological Bulletin

275

143

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Following a historical sketch of attempts to explain homosexuality, we review evidence indicating that the process of determining human sexual orientation is fundamentally the same in all mammals. In this process, four phenotypic dimensions of sexuality develop from two more or less distinct sex genotypes. Studies are reviewed that indicate how phenotypic deviations from these two genotypes (called sexual inversions) can occur. The causes of sexual inversions are categorized as genetic-hormonal, pharmacological, maternal stress, immunological, and social experiential. From this evidence, we propose a theory of how the entire spectrum of human sexual orientation (vs. simply homosexuality) is determined.A consistent preference for sexual relations with one's own sex (homosexuality), the opposite sex (heterosexuality), or vary-

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Section: Blocking or Augmenting The Effects Ofandrogens With Drugsmentioning

confidence: 99%

Neurohormonal functioning and sexual orientation: A theory of homosexuality–heterosexuality.

Ellis

Ames²

1987

Psychological Bulletin

275

143

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show abstract

“…Agents that interfere with the synthesis (e.g., estradiol-17/3), circulation, or action of testosterone (e.g., cyproterone acetate) block masculine differentiation of the genitalia of genetically male embryos, as manifested by the production of hypospadias-i.e., a displacement of the urethral orifice down the shaft of the penis from the tip with a shortening of the anogenital distance (2-10). The means by which testosterone organizes masculine differentiation of the genitalia in the embryo depends on classical androgen hormonal receptor mechanisms (5,9,11). However, the precise steps involved in this organizing action of testosterone in the embryo are not known.…”

mentioning

confidence: 99%

The arachidonic acid cascade is involved in the masculinizing action of testosterone on embryonic external genitalia in mice.

Gupta¹,

Goldman²

1986

Proc. Natl. Acad. Sci. U.S.A.

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We have evaluated whether the arachidonic acid cascade may be involved in the folding and fusion of the penis and scrotum in masculine differentiation, a possibility raised by recent observations of the involvement of the arachidonic acid cascade in the analogous embryonic processes of elevation and fusion of the palatal shelves and of folding and fusion of the neural tube. To test this hypothesis, during embryonic masculine differentiation in mice of the B1O.A strain, we administered certain agents that produce blockade of masculinization. We report that arachidonic acid can reverse the inhibition of masculine development in male embryos produced by estradiol-17/8 or by cyproterone acetate, an androgen receptor-site blocker, and that such reversal can be prevented by an inhibitor of cyclooxygenase, such as indomethacin. We have also found that agents that block the arachidonic acid cascade at the level of phospholipase A2 (cortisone, phenytoin) or at the level of cyclooxygenase (indomethacin, aspirin) also block masculine differentiation and that such antimasculinization is reversed by arachidonic acid. The masculinization of male embryos is inhibited by indomethacin and aspirin, and the masculinization of female embryos produced by exogenous testosterone is prevented by indomethacin. These findings provide evidence that the mechanism by which testosterone organizes the genitalia involves a role of the arachidonic acid cascade leading to prostaglandins at a critical period of development and that interference with testosterone synthesis or action leads to a teratogenic deficiency of arachidonic acid during this time in the genital anlagen.Mammalian embryos of either genetic sex have initially an indifferent genital tubercle, which develops into a penis and scrotum, if there is a functioning embryonic testis or if there is not, by administration of testosterone to the mother; otherwise, the inborn female program is expressed (1). Agents that interfere with the synthesis (e.g., estradiol-17/3), circulation, or action of testosterone (e.g., cyproterone acetate) block masculine differentiation of the genitalia of genetically male embryos, as manifested by the production of hypospadias-i.e., a displacement of the urethral orifice down the shaft of the penis from the tip with a shortening of the anogenital distance (2-10). The means by which testosterone organizes masculine differentiation of the genitalia in the embryo depends on classical androgen hormonal receptor mechanisms (5, 9, 11). However, the precise steps involved in this organizing action of testosterone in the embryo are not known.A clue to the possible nature of these steps has been given by evidence (12,13) suggesting that the arachidonic acid cascade leading to prostaglandins may be involved in the elevation and fusion of the embryonic shelves in differentiation of the palate. This suggestion is based on the findings that (i) arachidonic acid reverses both the incidence of cleft palate induced in mice and rats by glucocorticoids in vivo and th...

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“…Therefore, if the above mentioned assumption were true, the administration of a compound which has an ability to inhibit the binding of 5a-dihydrotestosterone to cytosol macromolecules from male hypophysis and brain would have to result in increased secretion of gonadotropin and also, paradoxically, in increased production of testosterone. Such a phenomena was already reported after treatment of cyproterone (Newmann et al, 1970).…”

Section: Endocrinolmentioning

confidence: 61%

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

et al. 1979

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Aspects of Androgen-Dependent Events as Studied by Antiandrogens

Cited by 136 publications

References 68 publications

Neurohormonal functioning and sexual orientation: A theory of homosexuality–heterosexuality.

Neurohormonal functioning and sexual orientation: A theory of homosexuality–heterosexuality.

The arachidonic acid cascade is involved in the masculinizing action of testosterone on embryonic external genitalia in mice.

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

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