Testosterone application decreases the capacity for ACTH and corticosterone secretion in a rat model of the andropause.
The culminating phase of ageing in males-andropause is characterized by enhanced activity of the hypothalamic-pituitary-adrenal axis and frequent glucocorticoid excess. In parallel, free testosterone deficiency provides the baseline hormonal milieu for the ageing male. The aim of this study was to illustrate (using diverse microscopic and biochemical methodologies) the effects of testosterone application on the capacity for adrenocorticotropic hormone (ACTH) and corticosterone secretion in a rat model of the andropause. Middle-aged Wistar rats were divided into sham-operated (SO; n=8), orchidectomized (Orx; n=8) and testosterone treated orchidectomized (Orx+T; n=8) groups. Testosterone propionate (5 mg/kg b.w./day) was administered for three weeks, while SO and Orx groups received the vehicle alone. ACTH cells and the adrenal cortex were stained using immuno-histochemical, immuno-fluorescent and histochemical procedures. Circulating concentrations of testosterone, estradiol, ACTH and corticosterone, as well as the adrenal tissue corticosterone levels were measured by immunoassays. Testosterone application led to increased (p<0.05) serum concentrations of sex steroids. Consequently, in Orx+T rats the ACTH cell nuclei volume increased (p<0.05) by 34%, while the volume density of ACTH cells and their relative intensity of fluorescence decreased (p<0.05) by 46% and 21%, respectively, in comparison with the corresponding parameters in the Orx group. Testosterone also induced vasodilatation in the adrenocortical zona fasciculata, and decreased (p<0.05) the ACTH concentrations and adrenal tissue corticosterone levels by 38% and 31%, respectively, compared to the Orx group. In conclusion, testosterone administration caused a decrease in the capacity for ACTH and corticosterone secretion in a rat model of the andropause.
Department of Cytology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Despot Stefan Blvd. 142, 11060 Belgrade, Serbia. Electronic address: avlada@ibiss.bg.ac.rs.
Vladimir
V
Ajdžanović
Department of Cytology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Despot Stefan Blvd. 142, 11060 Belgrade, Serbia.
Ivana
I
Jarić
Department of Cytology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Despot Stefan Blvd. 142, 11060 Belgrade, Serbia.
Jasmina
J
Živanović
Department of Cytology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Despot Stefan Blvd. 142, 11060 Belgrade, Serbia.
Branko
B
Filipović
Department of Cytology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Despot Stefan Blvd. 142, 11060 Belgrade, Serbia.
Nataša
N
Ristić
Department of Cytology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Despot Stefan Blvd. 142, 11060 Belgrade, Serbia.
Marko
M
Miler
Department of Cytology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Despot Stefan Blvd. 142, 11060 Belgrade, Serbia.
Verica
V
Milošević
D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000378:metabolism*; D047649:Andropause / Q000502:physiology*; D000818:Animals; D003345:Corticosterone / Q000097:blood / Q000378:metabolism*; D008297:Male; D023421:Models, Animal; D009919:Orchiectomy; D051381:Rats; D013739:Testosterone / Q000494:pharmacology*
D013739:Testosterone; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone
ACTH; Andropause; Corticosterone; Rats; Testosterone