An aromatase inhibitor or high water temperature induce oocyte apoptosis and depletion of P450 aromatase activity in the gonads of genetic female zebrafish during sex-reversal.

Dietary administration of a cytochrome P450 aromatase (P450arom) inhibitor (fadrozole) in genetic female juveniles of zebrafish (Danio rerio) was performed at 15-40 days post-hatching. The percentage of gonadal masculinization in the genetic all-females at 40 days post-hatching, treated with 0, 10, 100 and 1000 microg fadrozole g(-1) diet(-1) were 0, 62.5, 100 and 100%, respectively. Rearing at high water temperature in genetic all-females was performed at 15-25 days post-hatching. The percentage of gonadal masculinization in the genetic all-females at 40 days post-hatching, at water temperatures of 28.5, 35 and 37 degrees C were 0, 68.8 and 100%, respectively. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive oocytes of early diplotene and perinucleolar stages in fadrozole-treated genetic females (1000 microg g(-1) diet(-1)) were observed at 15-40 days post-hatching during sex-reversal. In contrast, apoptotic oocytes of early diplotene stage in high temperature-treated genetic females (at 35 and 37 degrees C) during sex-reversal and presumptive males of wild-type fish during sex differentiation were found at 15-27 days post-hatching. Our findings indicate that oocyte apoptosis, depletion of P450arom activity and differentiation of spermatogonia during gonadal sex-reversal are caused by treatments of aromatase inhibitor or high water temperature.