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Japanese eels are commercially valuable species in Asian aquaculture. This study evaluated whether salmon pituitary extract (SPE) or 17β-estradiol (E 2 ) treatment can induce cytotoxic activity in eel ovarian follicles. Follicular cells died after exposure SPE for 24-h culture in an  in vitro  culture. Moreover, the E 2  treatment also significantly reduced follicular cell counts. These results reveal that the inhibition of follicular cell numbers by SPE may occur through SPE-induced steroidogenesis. Results of a quantitative PCR analysis indicated that adding E 2  to the culture decreased  bcl2  and increased  dnmt1  mRNA expression in Japanese eel follicular cells after 24 h. The results of a promoter assay revealed that E 2  significantly increase  dnmt1  promoter activity through estrogen receptor-binding site. An  in silico  analysis predicted several putative transcription factors targeting the  bcl2  gene promoter region. Methylation of the  bcl2  promoter accounted for the downregulation of  bcl2  by E 2 -mediated  dnmt1 . The DNA methylation level of the  bcl2  gene was significantly higher in E 2 -treated follicular cells than that in the control group. Finally, the E 2 -induced hypermethylation pattern of the  bcl2  promoter and the reduction in follicular cell numbers were suppressed by adding an MTase inhibitor. Our findings demonstrate that estrogen has a negative effect on the reproductive system of female eels by regulating an epigenetic mechanism during artificial maturation.

Estrogen suppresses bcl2 expression through dnmt1 in Japanese eel ovarian follicle