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Fig. 2
B[a]P-treated embryos exhibit defective nervous system development. In situ hybridization staining was performed with a riboprobe against elavl3, a marker gene specifically expressed in telencephalon (te), hypothalamus (hy), midbrain (mb), midbrain hindbrain boundary (mhb) and plate (mhp) and hindbrain (hb) of the developing brain (A). (A–I) Zebrafish embryos exposed to 0 μM. (control, 01% DMSO), 10-μM B[a]P and 20-μM B[a]P were analyzed at 24 hpf. Embryos in (A–C) are shown from the lateral view; the red arrowheads indicate developmental defects in the midbrain (mb), and the hollow arrowheads indicate developmental defects in midbrain-hindbrain boundary (mhb); (D–F) Embryos are shown from the lateral view. The developing telencephalon (te; rectangles in (E,F)) was wider and the expression of elavl3 was weaker than in the control embryos; (G–I) Images are focused on the hindbrain (hb) region. The development of cranial ganglia (cg) was dose-dependently affected by B[a]P treatment; (J) Expression alteration of elavl3 in B[a]P was quantified by real-time quantitative RT–PCR (* p < 0.05, ** p < 0.01 compared with the control).