Effect of chronic castration on testosterone and estrogen binding to mouse kidney

The effects of prolonged castration on cytosol and nuclear androgen binding were studied in an attempt to explain the apparent resistance to androgen action observed in chronic castrates of various species. The mouse kidney was chosen for study because it is an androgen responsive tissue, extensively characterized, which does not atrophy following castration. Presence of estradiol receptors in the same tissue permitted us to compare the effects of castration on androgen and estrogen binding. Specific nuclear uptake of [³H]-testosterone was not different in kidney minces from 24 h, 1 week and 2 week castrate male mice. Four and 6 weeks after castration, however, a 2-fold increase in the number of available cytosol testosterone binding sites was observed. No changes in estrogen binding were found in chronically castrated male mice. Treatment with the nonaromatizable androgen, dihydrotestosterone, prevented these changes in androgen binding, whereas treatment with estradiol did not. These data indicate that androgen exposure is important in the regulation of androgen receptor activity in male mouse kidney. Whether the differences observed in prolonged castrates result from changes in receptor synthesis, processing or metabolism remains to be determined.