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This study focused on its developmental toxicity by using zebrafish embryos. Zebrafish embryos were exposed to different concentrations (1, 2.5, 5, 10\u2009\u03bc<jats:sc>m<\/jats:sc>) of AF from 2\u2009h post\u2010fertilization (hpf) to 72 hpf. At 72 hpf, two major developmental defects caused by AF were found, namely severe pericardial edema and hypopigmentation, when embryos were exposed to concentrations higher than 2.5\u2009\u03bc<jats:sc>m<\/jats:sc>. Biochemical detection of oxidative stress enzyme combined with expressions of a series of genes related to oxidative stress, cardiac, metal stress and pigment formation were subsequently tested. The superoxide dismutase activity was decreased while malondialdehyde content was accumulated by AF treatment. The expression of oxidative stress\u2010related genes (<jats:italic>sod1<\/jats:italic>, <jats:italic>gpx1a<\/jats:italic>, <jats:italic>gst<\/jats:italic>), pigment\u2010related genes (<jats:italic>mitfb<\/jats:italic>, <jats:italic>trp\u20101a<\/jats:italic>) and one metal stress\u2010related gene <jats:italic>ctr1<\/jats:italic> were all decreased by AF exposure. The expressions of cardiac\u2010related genes (<jats:italic>amhc<\/jats:italic>, <jats:italic>vmhc<\/jats:italic>) and one metal\u2010related gene <jats:italic>hsp70<\/jats:italic> were found to be significantly upregulated by AF exposure. These findings indicated the potential developmental toxicity of AF on zebrafish early development. 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