Fish embryos and fry are known to be particularly sensitive to dioxins, particularly developmental processes. Symptoms of dioxin exposure in fish embryos and fry include edema of the yolk sac and pericardium, hemor-rhaging in the head and tail regions, craniofacial deformities, and wasting syndrome. The cardiovascular system, in particular the vascular endothelium of the developing embryo, has been identified as a primary target of dioxin-induced toxicity. Several other tissues, including gill and digestive tract, are also known target tissues for AhR agonists.
The developing embryos of oviparous vertebrates, such as fish, are particularly prone to the adverse effects of dioxins due to their elevated exposure risk through water, sediment, and dietary sources of dioxin. Dioxin exposure has led to reduced and, in some cases, failed recruitment of young fish into breeding populations, which is believed to have occurred in lake trout in the Great Lakes, USA, during the 1960s and 1970s.
Dioxin toxicity in fish tends to be higher for congeners containing four, five, or six chlorine atoms. It appears that congeners with fewer chlorine atoms tend to be more rapidly metabolized and eliminated, while more highly chlorinated compounds have limited membrane permeability or bioavailability. As with higher mammal studies, it appears that 2,3,7,8-TCDD is the most toxic congener to juvenile and adult fish. Fish eggs appear to be highly sensitive, and likely represent the most important route of exposure for early life stages.
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