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Androgens control androgen-binding sites in rat epididymis
Endocrinology
|September 1, 1983
Summary
Androgen deprivation significantly reduces androgen receptor binding sites in rat epididymis. Testosterone replacement therapy restores these sites, indicating androgen control over receptor levels and nuclear translocation.
Area of Science:
- Endocrinology
- Molecular Biology
- Reproductive Biology
Background:
- Androgen-binding sites in the epididymis are crucial for male reproductive function.
- Previous studies suggested androgen regulation of these sites.
Purpose of the Study:
- To investigate the dynamic changes in androgen receptor number and affinity in rat epididymis following castration and androgen replacement.
- To explore the impact of androgens on receptor translocation and epididymal cell populations.
Main Methods:
- Utilized an exchange technique for receptor determination in rat epididymis.
- Measured cytoplasmic and nuclear androgen receptor binding sites and affinity (Kd) using [3H]methyltrienolone.
- Assessed the effects of castration and testosterone propionate administration on receptor levels, DNA synthesis, and proteolytic activity.
Main Results:
- Castration led to a significant decrease in cytoplasmic and nuclear androgen receptor numbers, with reduced affinity observed in cytoplasmic receptors.
- Testosterone propionate administration restored both cytoplasmic and nuclear receptor levels.
- Androgen treatment increased labeled thymidine incorporation into DNA and elevated the proportion of translocatable binding sites.
Conclusions:
- Androgen levels critically control the number of androgen receptor binding sites in the rat epididymis.
- Androgens influence receptor translocation into the nucleus and stimulate DNA synthesis.
- The study suggests heterogeneity within the cytoplasmic androgen receptor population.