Effects of combined stressors to TCDD and high temperature on HSP/CYPs signaling in the zebrafish embryos/larvae.

Global warming causes the release of dioxin-like deposits and increases geographical migration, increasing the risk of exposure for humans and animals. In this experiment, we used CYP1A transgenic zebrafish Tg (cyp1a: mCherry) and liver fluorescent transgenic zebrafish Tg (fabp10: Ps Red) as an animal model and exposed to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) at 26 °C and 30 °C, respectively. Morphological changes, histological changes, transcriptome and related genes expression were detected. The results showed that exposure to TCDD at 30 °C increased the mortality rate, pericardial cavity area, and reduced the number of liver cells in zebrafish larvae compared to 26 °C. Transcriptome analysis showed that, TCDD significantly altered Peroxisome Proliferators-Activated Receptors (PPARs) metabolic pathway, adipocytokine, fatty acid degradation and cell death. qRT-PCR also detected a further significant increase in the expression of ahr2, cyp-related genes (cyp1.1, cyp1b1, cyp1c1 and cyp3a65), and PPARs (pparα, pparβ and pparγ) in zebrafish larvae induced by TCDD exposure under 30 °C compared to 26 °C water temperature incubation. Our results showed that the increase of ambient temperature (from 26 °C to 30 °C) causes TCDD induced hepatotoxicity to be more intense. The observed toxic changes were likely related to lipid peroxidation.