The hormone 17β-estradiol (E2) can be found in rivers, effluents, and even drinking water. Researches have demonstrated that E2 affects various metabolic pathways through gene activation and may cause reproductive toxicity in fish. Therefore, the aim of this study was to evaluate E2-induced toxicity via testicular transcriptome of zebrafish (Danio rerio) exposed to different concentrations (10 ng L-1, and 100 ng L-1) of E2. A total of >600 significant differentially expressed genes (DEGs) were enriched among the three treatments. Short time-series expression miner analysis revealed five KEGG pathways including drug metabolism, other enzymes, calcium signaling pathway, ECM-receptor interaction, gap junction, and cell adhesion molecules. Twenty genes were selected to verify the accuracy of RNA-Seq. Other reported genes related to sex differentiation, development, energy metabolism, and other processes were found. One set of genes significantly increased/decreased/fluctuated over time, especially 12 h after E2 exposure. Genes associated with ovaries (zp3c), and development (bmp15, gdf9, and sycp2l) were significantly upregulated with increasing E2 concentration. E2 and testosterone was significantly decreased by 10 (except for T) and 100 ng L-1 E2 exposure at 12 h. The current study demonstrated that sex differentiation, development, energy metabolism, immunity, and ribosome biogenesis in male zebrafish were all significantly affected by 17β-estradiol exposure through transcriptional alterations.
Keywords: 17β-estradiol; Follicular development; Ribosome biogenesis; Sex differentiation; Testicular transcriptome.
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