FIGURE SUMMARY
Title

The Effect of the Pyrethroid Pesticide Fenpropathrin on the Cardiac Performance of Zebrafish and the Potential Mechanism of Toxicity

Authors
Saputra, F., Lai, Y.H., Roldan, M.J.M., Alos, H.C., Aventurado, C.A., Vasquez, R.D., Hsiao, C.D.
Source
Full text @ Biology (Basel)

Mortality rate of zebrafish embryos after incubation in several concentrations of fenpropathrin and the LC50 value. Red line show the non-linear curve for the LC50 calculation.

Ventricle chamber of the control group (A) and 1-ppm-treated group (B) after 24 h of incubation in fenpropathrin at the end of the diastolic phase. Yellow lines show the outline of the ventricle chamber. Cardiac performance parameters after 24 h of acute incubation in different concentrations of fenpropathrin from 0.01 to 1 ppm (CI). The data were presented as mean ± statistical error mean (SEM), and the statistical significance was calculated using Ordinary One-Way ANOVA with Dunnet multiple comparison test. (** p < 0.01, *** p < 0.001, **** p < 0.0001).

Condition of the dorsal aorta of control group (A) and the 1 ppm fenpropathrin-treated group (B). The yellow line represents the border of the dorsal aorta, while the red box represents its position for high-speed videography. (C) The blood flow velocity profile in the dorsal aorta following incubation in fenpropathrin concentrations of either zero (black), 0.01 (green), 0.1 (yellow), or 1 ppm (orange). (D) Maximum blood flow velocity, (E) average blood flow velocity, and (F) dorsal aorta diameter following 24 h of acute incubation in fenpropathrin. The data were presented as mean ± SEM, and the statistical significance was determined using Ordinary One-Way ANOVA with the Dunnet multiple comparison test. (**** p < 0.0001).

Oxygen consumption rate of zebrafish after exposure to fenpropathrin. The left graph depicts the oxygen level over time, showing a clear increase in oxygen consumption. The right graph shows the total oxygen consumption of zebrafish at the end of the test, which was significantly higher for fenpropathrin-exposed group compared to control group. Two-Way ANOVA was conducted to calculate the significant difference in the oxygen level over time between each treatment, and Geisser–Greenhouse correction was performed for multiple comparison tests. The data for total oxygen consumption were presented as mean ± SEM, and the statistical significance was calculated using Ordinary One-Way ANOVA with Dunnet multiple comparison test. (n = 46, * p < 0.05, **** p < 0.0001).

Graphical representation of the binding position of fenpropathrin into voltage-gated calcium (cacna1sb (A)), chloride (clcn3 (B)), and sodium channel (scn1lab (C)) and apoptosis-related gene bcl2a (D) and p53 (E). The dashed red line shows the position of fenpropathrin.

Graphical representation of the binding position of fenpropathrin into voltage-gated calcium (cacna1sb (A)), chloride (clcn3 (B)), and sodium channel (scn1lab (C)) and apoptosis-related gene bcl2a (D) and p53 (E). The dashed red line shows the position of fenpropathrin.

Expression of genes related to cardiovascular development after exposure to fenpropathrin. The data were presented as mean ± SEM, and the statistical significance was calculated using Ordinary One-Way ANOVA with Dunnet multiple comparison test. (n = 4, * p < 0.05, ** p < 0.01, **** p < 0.0001).

Proposed mechanism of fenpropathrin-induced cardiovascular toxicity in zebrafish. The physiological evidence was collected from cardiovascular and metabolic assays and is highlighted in red. The molecular evidence was collected from mRNA expression assay and is highlighted in blue. Some indirect evidence collected from molecular docking is highlighted with dotted arrow.

Acknowledgments
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