Fig. 2

The (A) developmental malformations and (B) malformation rates in zebrafish embryos exposed to indicated concentrations of DPE at 24 and 48 hpf. GR, general retardation; HT, helical tail; EA, eye alteration. Retinoic acid was employed as a positive control.

Fig. 3

Effect of DPE on cell death in zebrafish embryos. (A) The cell death levels were measured after acridine orange staining by image analysis and fluorescence microscopy. (B) Individual zebrafish fluorescence intensity was quantified using an image J program. The values are expressed as the mean ± SE.

Fig. 4

Inhibitory effect of DPE on lipopolysaccharide (LPS)-stimulated ROS production in zebrafish embryos. (A) The ROS levels were measured after staining with DCF-DA by image analysis and fluorescence microscopy. (B) Individual zebrafish fluorescence intensity was quantified using an image J program. The values are expressed as the mean ± SE. Significant differences from the only LPS-treated group were identified at * p < 0.05.

Fig. 5

Protective effect of DPE on LPS-stimulated cell death in zebrafish embryos. (A) The cell death levels were measured after staining with acridine orange by image analysis and fluorescence microscopy. (B) Individual zebrafish fluorescence intensity was quantified using an image J program. The values are expressed as the mean ± SE. Significant differences from the only LPS-treated group were identified at * p < 0.05.

Fig. 6

Inhibitory effect of DPE on LPS-stimulated NO production in zebrafish embryos. (A) The NO levels were measured after staining with DAF-FM-DA by image analysis and fluorescence microscopy. (B) Individual zebrafish fluorescence intensity was quantified using an image J program. The values are expressed as the mean ± SE. Significant differences from the only LPS-treated group were identified at * p < 0.05.

Acknowledgments
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