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Studying Neurobehavioral Effects of Environmental Pollutants on Zebrafish Larvae
Published on: February 5, 2020
2,4,6-tris(2,4,6-tribromophenoxy)-1,3,5-triazine (TTBP-TAZ) exposure can cause cardiac toxicity in zebrafish larvae
1Hubei Key Laboratory of Environmental and Health Effects of Persistent Toxic Substances, School of Environment and Health, Jianghan University, Wuhan, 430056, China.
Abstract:
2,4,6-tris(2,4,6-tribromophenoxy)-1,3,5-triazine (TTBP-TAZ) is a widely used novel brominated flame retardant with environmental persistence, yet its developmental toxicity remains poorly characterized. In this study, we investigated the developmental and cardiotoxic effects of TTBP-TAZ in zebrafish embryos/larvae. Embryos (4 hpf) were exposed to 0-20 μM TTBP-TAZ for 120 hpf. Assessments included survival, hatching kinetics, burst activity (24 hpf), heart rate (48 hpf), caudal venous blood-flow velocity (72 hpf), locomotor behavior under alternating light/dark conditions (120 hpf), cardiac morphology in Tg(myl7:EGFP), and transcription of key cardiac genes. Results indicated low mortality of embryos/ larvae across all concentrations. However, TTBP-TAZ accelerated hatching rate in a concentration-dependent manner (significant by 60 hpf) and increased burst activity. Elevated heart rate (48 hpf) and enhanced tail-vein blood flow (72 hpf) suggested tachycardia and stimulated circulation. Transgenic larvae exhibited reduced ventricular/atrial fluorescence intensity, along with enlarged cardiac size and indistinct contours, indicating structural abnormalities. qPCR analysis revealed up-regulation of nkx2.5, tbx20, and vmhc, and down-regulation of gata4, mef2, and myh7, suggesting disruption of core cardiogenic transcription and chamber-specific contractile programming. Locomotor assays demonstrated hyperactivity at higher concentrations under both light and dark conditions. These findings indicate sub-lethal TTBP-TAZ exposure induces significant developmental and cardiotoxic disturbances in zebrafish, associated with altered cardiac gene expression and functional hyperactivation. This study supports the need for further mechanistic investigation and exposure-relevant risk assessment of TTBP-TAZ.

