ANDROGEN-DEPENDENT MAST-CELL DEGRANULATION IN THE HARDERIAN-GLAND OF FEMALE SYRIAN-HAMSTERS - IN-VIVO AND ORGAN-CULTURE EVIDENCE

In previous articles we have reported the ''disappearance'', of Harder ian gland mast cells (HGMC) after treatment with testosterone. In the present work we study: (a) if the apparent decrease in the number of m ast cells caused by this androgen is real or is due to the fact that t estosterone induces mast cell degranulation that avoids its recognitio n by toluidine blue staining; (b) if testosterone acts through its rec eptor directly on the Harderian gland (HG). In order to give an answer to the first question, we observed HG of female Syrian hamsters treat ed with testosterone under the electron microscope to find the possibl e degranulated mast cells not recognizable with the aid of the toluidi ne blue staining. We also studied in vivo and in vitro the effects of the beta-agonists isoproterenol and salbutamol, given that they increa se cAMP and can therefore prevent degranulation of mast cells. Finally we have used cytocalasin B, which inhibits degranulation by blocking actin depolimerization. Both the beta-agonists and cytochalasin B were able to prevent the decrease of mast cells, as recognized by staining with toluidine blue after treatment with testosterone. Indeed, when o bserved under the electron microscope, abundant degranulated mast cell s were found after treatment with testosterone. For solving the second issue we analyzed the effect of the antiandrogen cyproterone acetate in vivo and in vitro. Our results demonstrate that testosterone is abl e to induce degranulation of HGMC in the Syrian hamster Mesocricetus a uratus and that this effect is achieved directly through its receptor on the Harderian gland.