John Wiley & Sons, Ltd.

Embryonic exposure to 2,3,7,8‐TCDD impairs prey capture by zebrafish larvae

2,3,7,8‐TCDD remains a ubiquitous, persistent environmental contaminant with the potential for causing lethal deformities in larval fishes. Few studies have examined its impacts on larval growth and craniofacial development in conjunction with feeding capability. Here we use morphological and behavioral assessments to demonstrate that feeding capability of larvae is impaired even when craniofacial structures are not grossly malformed. Zebrafish embryos were exposed to 25, 50 or 100 pg TCDD/ml or <0.1% DMSO for one hour at 4 h post fertilization (hpf), and then raised in clean water for 21 or 90 days to assess craniofacial morphology, feeding capability and long‐term survival. The lower jaw was 5% smaller in 21‐day larvae exposed to ≥ 50 pg TCDD/ml, and those larvae caught 10% fewer prey items; survival was reduced by 13–23%. The direct cause of TCDD's impacts on feeding capability is not known, but feeding success was correlated with growth, length of lower jaw, and survival. Since low larval mortality rates are key for recruitment, this suggests that exposure to concentrations of TCDD during embryonic development that do not initially cause mortality still have the potential for impacting recruitment success of feral fish. Further, this work provides additional evidence that behavioral endpoints are often more sensitive than morphological ones, and should be included when assessing the sublethal toxicity of environmental contaminants. Environ Toxicol Chem © 2013 SETAC

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