Hormone regulation of the rodent Harderian gland: binding properties of the androgen receptor in the male golden hamster

in Journal of Endocrinology
Authors:
F. Vilchis
Search for other papers by F. Vilchis in
Current site
Google Scholar
PubMed
Close
,
A. Hernandez
Search for other papers by A. Hernandez in
Current site
Google Scholar
PubMed
Close
,
A. E. Perez
Search for other papers by A. E. Perez in
Current site
Google Scholar
PubMed
Close
, and
G. Perez-Palacios
Search for other papers by G. Perez-Palacios in
Current site
Google Scholar
PubMed
Close
Restricted access
Rent on DeepDyve

Sign up for journal news

ABSTRACT

Studies were conducted in castrated golden hamsters to assess whether sexual dimorphism and sensitivity to sex steroid hormones in the rodent Harderian gland are mediated by an interaction of androgens with specific intracellular receptors. Physical properties, binding kinetics and stereospecificity of the androgen receptor were analysed using [3H]mibolerone as the radioligand. The presence of [3H]mibolerone–androgen receptor complexes with a sedimentation coefficient of 7–8S was demonstrated in Harderian gland cytosol by a linear sucrose gradient ultracentrifugation technique using a vertical rotor. Kinetic analysis revealed an androgen-binding site with an apparent dissociation constant of 0·3±0·07 (s.d.) nmol/l and a saturation binding capacity of 113±15 fmol/mg protein. Displacement studies indicated that unlabelled mibolerone, methyltrienolone, 5α-dihydrotestosterone and testosterone were efficient competitors for the androgen-binding sites, while progesterone, 17β-oestradiol, dexamethasone, dehydroepiandrosterone, ethiocholanolone and 5α-16-androsten-3-one were not. Experiments in long-term castrated animals revealed that the Harderian gland androgen receptor concentration and sedimentation coefficient remained unmodified. The results of these studies were interpreted as demonstrating the presence of a specific high-affinity intracellular androgen receptor in the male hamster Harderian gland.

J. Endocr. (1987) 112, 3–8

 

  • Collapse
  • Expand