PubMed · 61663
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W Krause. 1976-05-15. [Indications and supervision of therapy with anti-androgens].. https://pubmed.ncbi.nlm.nih.gov/61663/
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Cyproterone acetate, R 2956, Ro 7-2340 and Sch 13521 in the daily dose of 8 mg injected intramuscularly to castrated adult hamsters for 3 weeks were all found to significantly antagonize the stimulatory effect of exogenous testosterone propionate (80 microgram im, every other day) on the sebaceous gland as well as the prostate and the seminal vesicle. With a view to clarifying the mechanisms of action of these antiandrogenic drugs on the sebaceous gland, the present author carried out both in vivo and in vitro experiments and examined how they would interfere with the binding of 3H-dihydrotestosterone (DHT) to cytosol and nuclei. When 200-1000 excess quantities of the antiandrogens were administered to the experimental animals 10 min before injection of 3H-testosterone, all of them except R 2956 reduced the bound radioactivity in the nuclei of the sebaceous gland by more than 40%. Incubation of the cytosol fraction with 1 x 10(-7) M of cyproterone acetate caused a 70% decrease in radioactivity of the specific binding. In contrast, such inhibitory activities of the three other antiandrogens were less conspicuous even at 1 x 10(-6) M. In the homogenate of the sebaceous gland incubated with 1 x 10(-8) M of DHT, the other drugs than Sch 13521 curbed the characteristic binding of DHT to macromolecules of the nuclei by nearly 70% at 1 x 10(-6) M.
Studies in vitro and in vivo indicate that steroid secretion by granulosa cells of the developing follicle is modulated in part by steroid hormones themselves. Androgens stimulate progestin synthesis in vitro by granulosa cells of all developmental stages independently of their role as an estrogen precursor; generally, the action of estradiol results in suppression of progesterone secretion. The nature of the relationship between steroid secretion by granulosa cells and the physiological processes of follicular development or atresia remains to be investigated in greater detail. The cellular mechanism(s) of steroidal modulation of steroid secretion is unknown but apparently does not involve changes in the number of granulosa cell LH receptors per se.
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