Key Event Overview
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AOPs Including This Key Event
|AOP Name||Event Type||Essentiality|
|AhR activation leading to embryo toxicity in fish||AO|
|Aryl hydrocarbon receptor activation leading to embryolethality via cardiotoxicty||KE||Strong|
Level of Biological Organization
How this Key Event works
Severe cardiac dysfunction can result in congestive fetal heart failure (inability of the heart to deliver adequate blood flow to organs) leading to fluid build-up in tissues (in this case, the pericardium) and cavities (edema and effusion, respectively). Fluid buildup exerts a positive pressure on cardiac chambers, which limits the diastolic ventricular filling reserve and diminishes cardiac output (Thakur et al. 2013).
How it is Measured or Detected
In experimental studies, edema is often scored as present or absent rather than being measured quantitatively. The severity of the edema can be scored based on the area of the pericardial cavity, which can be estimated using CT, ultrasound or MRI equipped with imaging software. This technique has been demonstrated by Prasch et al. (2003) in zebrafish to quantify the pericardial sac area.
Evidence Supporting Taxonomic Applicability
Birds, fish and mammals are susceptible to pericardial edema.
1. Prasch, A. L., Teraoka, H., Carney, S. A., Dong, W., Hiraga, T., Stegeman, J. J., Heideman, W., and Peterson, R. E. (2003). Aryl hydrocarbon receptor 2 mediates 2,3,7,8-tetrachlorodibenzo-p-dioxin developmental toxicity in zebrafish. Toxicol. Sci. 76(1), 138-150.
2. Thakur, V., Fouron, J. C., Mertens, L., and Jaeggi, E. T. (2013). Diagnosis and management of fetal heart failure. Can. J Cardiol. 29(7), 759-767.
Tal, TL et al. Immediate and long-term consequences of vascular toxicity during development using a quantitative vascular disruption assay in zebrafish. Manuscript in preparation.