Initiation of Precocious Sexual Maturation in the Immature Rat Treated with Dehydroepiandrosterone¹

Abstract

The normal weight increase of the epididymis during sexual maturation and its maintenance through adulthood were found to be dependent on the provision of androgens. Binding of [3H]dihydrotestosterone (DHT) to the epididymal 8S cytoplasmic receptor gradually decreased after castration to become undetectable after 25 days. Binding to the androgen binding protein (ABP) was absent 4 days after castration and was not reinduced by 3 weeks of testosterone (T) administration. Unilateral castration for periods of up to 27 days showed the disappearance of ABP with preservation of the 8S receptor on the castrated side, indicating a testicular source for ABP and the epididymal origin of the 8S receptor. The tissue concentrations of T and DHT in the epididymis became undetectable 30 days after castration and were restored to normal values by administration of testosterone in large doses (1.5 mg/100 g BW). Similar results were obtained in rats castrated at 10 days of age and injected with testosterone until 60 days old. The ratio DHT/T was depressed in the castrate and increased with testosterone treatment. The protein content of the epididymis (mg of protein/g wet weight) was also found to be influenced by androgens. Our results show evidence of some mechanisms involved in the trophic effect of androgens upon the epididymis and suggest the possible androgenic control of epididymal 5alpha-reductase activity. They also indicate that a testicular factor is required for the maintenance of the 8S cytoplasmic androgen receptor. It is not known whether this factor is testosterone or some other testicular secretion.

Effects of Acute Stanozolol Treatment on Puberty in Female Rats1

“…There is no evidence in the literature that the AR is involved in the advancement of VO. Contrary to the actions of estrogen and aromatizable androgens, nonaromatizable androgens either have no effect on the onset of puberty or delay it [9,10]. Taken together, the results of the present experiments suggest that stanozolol may be acting at the vaginal ER to advance VO.…”

“…In contrast to the advancement of puberty by estrogen and aromatizable androgens, treatments with nonaromatizable androgens delay the onset of puberty [9,10]. Thirty-day treatment with one AAS, stanozolol, has differential effects on pubertal endpoints in female rats.…”

Effects of dehydroepiandrosterone, Premarin and Acolbifene on histomorphology and sex steroid receptors in the rat vagina

“…Other studies using co-administration of DHEA and the antiestrogen Acolbifene or the antiandrogen FLU, respectively, have demonstrated that the action of DHEA in the rat mammary gland [42], skin sebaceous glands [43] and bone mineral density [44] is almost exclusively androgenic. Nevertheless, the presence of an estrogenic action of DHEA in the rat vagina has been previously demonstrated, either by the formation of a stratified epithelium in the vagina of rats treated with FLU and DHEA (unpublished data), or through induction of vaginal opening and precocious ovulation in immature rats treated with this compound, while DHT, an androgen not aromatizable to estrogens, did not produce such effects [45]. The capacity of rat vaginal tissue to aromatize androgens, especially, Testo, is likely to account for the major part of the estrogenic effect of DHEA in this organ [46].…”

Influence of Dehydroepiandrosterone on the Expression of Insulin-Like Growth Factor-1 during Cystogenesis in Polycystic Rat Ovaries and in Cultured Rat Granulosa Cells1

“…Subsequent studies confirmed that the DHEA-PCO rat model exhibits many of the salient features of human PCO. The administration of DHEA induces cystic changes in the ovaries of immature female rats, in conjunction with precocious ovulation, acyclicity, and anovulation [9][10][11]. Similarly, ovarian cysts are noted when DHEA is given to adult cycling rats [12].…”