John Wiley & Sons, Ltd.

Cardiac toxicity by sublethal 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin correlates with its anti‐proliferation effect upon cardiomyocytes in zebrafish embryos

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The cardiac toxicity of zebrafish embryos in response to the lethal dose of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) has been well characterized. However dioxin contamination levels in nature are usually lower and sublethal TCDD toxicity is less investigated. We found that for the 72 hours post fertilization (hpf) zebrafish embryos, the non‐lethal doses of TCDD were 25 pg/ml and lower. 10 pg/ml and 25 pg/ml TCDD concentrations were determined to be used in our sublethal TCDD study. Characterization of their toxicity was then followed. The results showed that at these two dosages, embryos still exhibited acute and subchronic cardiac toxicity. The stroke volume and cardiac output of these embryos significantly declined early until 8d post exposure. Their heart size became smaller. The hearts of these embryos contained less total number of cardiomyocytes per heart with decreased cardiomyocyte proliferation. Apoptosis was not detected either in the TCDD treated or in the control hearts. Real‐time PCR revealed the transcription of a battery of cell‐cycle related genes was suppressed within the sublethal TCDD treated heart. On the contrary, embryonic jaw development seemed not to be affected. The present study suggests that dioxin contamination, even at lower levels, might still lead to cardiac toxicity in fish embryos. Such cardiac toxicity presents as disrupted normal heart function, originating from the anti‐proliferative effect of sublethal TCDD upon cardiomyocytes. This article is protected by copyright. All rights reserved

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