Adrenocortical influence on histokinetics and lipid components of uropygial gland of immature chick.

Adrenocortical influence on uropygial gland of 10-day old male white leghorn chicken was assessed by suppressing glucocorticoid level with metyrapone and following corticosterone and deoxycorticosterone acetate (DOC) treatments (im), 100 micrograms each on alternate day for a period of 15 days. Metyrapone treatment resulted in significant atrophy of the uropygial gland with a severe regression of the glandular alveoli due to cytopycnosis, cellular disintegration and drastic cell loss. Concomitantly, there was a depletion of glandular lipid and its diester wax fraction. Corticosterone, administered simultaneously with metyrapone, counteracted severe adverse effects of the latter on the uropygial gland. In the normal chicken also corticosterone alone caused glandular hypertrophy with increased rate of cell renewal and cell growth within the alveoli and, to a lesser extent, augmented output of the glandular lipids. Simultaneous administration of corticosterone and testosterone propionate (TP), on the other hand, caused a moderate suppressive influence on this gland. DOC treatment alone or with metyrapone and TP failed to exert any noteworthy change in the uropygial gland excepting a moderate reduction of gland weight and a rise of glandular lipids observed after combined injections of DOC with TP and with metyrapone respectively.

Alteration in the histochemical profile of steroid dehydrogenases in the uropygial gland of male domestic pigeons following androgen deprivation and testosterone supplement.

Activities of delta 5-3 beta-hydroxysteroid dehydrogenase (3 beta-HSDH) and 17 beta-hydroxysteroid dehydrogenase (17 beta-HSDH)) were histochemically demonstrated in the alveoli of the uropygial glands of male domestic pigeons (Columba livia Gmelin). The level of 3 beta-HSDH (Substrates: pregnenolone and dehydroepiandrosterone) was very low. On the other hand, an intense activity of 17 beta-HSDH was observed in the glandular alveoli of both sexually immature and adult pigeons when testosterone was used as the substrate. In the adult specimens, bilateral castration resulted in a moderate increase of the level of 17 beta-HSDH indicating a faster rate of conversion of testosterone into the weaker androgen, namely, delta 4-androstene-3,17-dione. On the other hand, administration of testosterone propionate (TP), 500 micrograms/bird/day for 15 days in the intact prepubertal and castrated adult pigeons caused a perceptible depletion of 17 beta-HSDH, which may be correlated with the increase in the local concentration of testosterone. Low dose of TP (100 micrograms/day) had no effect. When estradiol-17 beta was used as the substrate for 17 beta-HSDH, there was only a feeble response within the alveoli.

Action of estriol on the uropygial gland activity in pigeon.

Administration of estriol (Sigma Chemical Co., U.S.A.) in the female young-adult pigeons at a dose of 50 micrograms/bird/day for 7 consecutive days caused atrophy of the uropygial gland, associated with increased cytopycnosis and drastic cell loss within the holocrine alveoli and reduction in the content of the glandular lipids. Probable mode of action of this steroid upon the uropygial gland has been suggested in the light of the recent data on its anti-estradiol property manifested in rat uterus.