Ovarian pieces containing postvitellogenic follicles were incubated in vitro with different concentrations of the catecholestrogen 2-hydroxyestradiol-17β (2-OHE(2)) to evaluate its effects on steroid production and germinal vesicle breakdown (GVBD) in the catfish Heteropneustes fossilis. The incubation with 2-OHE(2) induced a shift in steroidogenic pattern: the C(19) and C(18) steroids testosterone (T) and estradiol-17β (E(2)), respectively were significantly decreased with a concomitant significant increase in the C(21) steroids progesterone (P(4)), 17-hydroxyprogesterone (17-OHP), 17,20β-dihydroxy-4-pregnen-3-one (17,20β-DP), 17,20α-dihydroxy-4-pregnen-3-one (17,20α-DP) and cortisol (F). Concomitantly, the catecholestrogen induced dose-dependently GVBD response, the first sign of meiosis resumption. The co- and pre-incubations of the ovarian pieces with 2-OHE(2), and adrenergic (phentolamine, α-blocker and propranolol, β-blocker) or estrogen (tamoxifen) receptor blockers resulted in inhibition of the stimulatory effect of the catecholestrogen on C(21) steroids and reversed the inhibition of testosterone and E(2). The α-blocker was more effective than the β-blocker. Our results suggest that 2-OHE(2) appears to employ both adrenergic (α-type) and estrogen receptor mechanisms in mediating the effects. The co- or pre-incubation of ovarian pieces with IBMX (a cAMP elevating drug), H89 (a protein kinase A inhibitor), and PD098059 (a MAP kinase kinase inhibitor) significantly inhibited the stimulatory effect of 2-OHE(2) on the C(21) steroids. The effect of chelerythrine (a protein kinase C inhibitor), on the other hand, varied with the incubation condition. In the co-incubation, the steroids showed varied effects: 17,20β-DP, testosterone and E(2) were elevated, and P(4) and 17-OHP were decreased. In the pre-incubation set up, all the steroids were inhibited except E(2). The inhibition by the blockers was higher in the pre-incubation groups. Taken together, the data suggest the involvement cAMP-protein kinase A, protein kinase C and MAP kinase pathways in the modulation of the steroidogenic activity.
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