Effect of pituitary hormones, androgens, and corticosteroids on the seminal vesicles of the castrate catfish, Heteropneustes fossilis (Bloch).

Abstract

AbstractΔ5‐3β‐hydroxysteroid dehydrogenase activity (Δ5‐3β‐HSD) has been studied in the interrenal glands and the seminal vesicles of intact and castrate male catfish. The intensity of the enzyme reaction is about equal in the seminal vesicles of both groups, whereas the intensity of enzyme reaction in the cortical cells is more pronounced in the castrate than in the intact male.The responses of the interrenal glands and the regressed seminal vesicles of the castrate catfish in the postspawning period to exogenous luteinizing hormone (LH), Δ4‐androstenedione (Δ4‐androst.), desoxycorticosterone acetate (DCA) and hydrocortisone acetate (HA) (experiment 2), and the effect of the LH, Δ4‐androst., DCA and HA, and prolactin (LtH) and growth hormone (STH), singly or in combination on the regressed seminal vesicles of the castrate catfish (experiment 3) have also been studied. The data indicate that both LH and Δ4‐androst. induce secretory activity in the seminal vesicles but they appear to act through different routes. Since LH brings about an increase in the nuclear diameters in cortical cells and Δ4‐androst. does not, it is felt that LH acts through the cortical cells of the interrenal glands while Δ4‐androst. acts directly on the seminal vesicles. Further, Δ4‐androst. can synergize with LtH and STH in inducing secretory activity in the seminal vesicles, whereas DCA and HA do not. These results, coupled with the fact that Δ5‐3β‐HSD activity is more marked in the cortical cells of the castrate than in the intact catfish, strongly suggest that following castration, the resulting high titers of gonadotrophin act on the interrenal cortical cells to produce androgens which, in turn, induce hyperactivity in the seminal vesicles.