Abstract

Background2,2′,4,4′-Tetrabromodiphenyl ether (BDE47) is a prevalent environmental pollutant and has been demonstrated to be a serious toxicant in both humans and animals, but little is known about the molecular mechanism underlying its toxic effect on the early development of vertebrates. BDE47-treated zebrafish larvae were found to present the light-related locomotion reduction in our previous study, therefore, we aimed to use high throughput sequencing to investigate the possible reasons from a transcriptomic perspective.ResultsBy exposing zebrafish embryos/larvae to 5 μg/l and 500 μg/l BDE47, we measured the influence of BDE47 on the mRNA expression profiles of zebrafish larvae until 6 days post-fertilization, using Illumina HiSeq 2000 sequencing. Differential expression analysis and gene enrichment analysis respectively revealed that a great number of genes, and gene sets based on two popular terminologies, were affected by the treatment of 500 μg/l BDE47. Among them, BDE47 caused changes in the retinal metabolism and related biological processes involving eye morphogenesis and visual perception, as confirmed by disordered photoreceptor arrangement and thickened bipolar cell layer of larval retina from histological observations. Other altered genes such as pth1a and collaborative cathepsin family exhibited disrupted bone development, which was consistent with the body curvature phenotype. The transcriptome of larvae was not significantly affected by the treatment of 5 μg/l BDE47, as well as the treatment of DMSO vehicle.ConclusionsOur results suggest that high BDE47 concentrations disrupt the eye and bone development of zebrafish larvae based on both transcriptomic and morphological evidences. The abnormal visual perception may result in the alteration of dark adaption, which was probably responsible for the abnormal larval locomotion. Body curvature arose from enhanced bone resorption because of the intensive up-regulation of related genes. We also proposed the larval retina as a novel potential target tissue for BDE47 exposure.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-014-1194-5) contains supplementary material, which is available to authorized users.

Highlights

  • Polybrominated diphenyl ethers (PBDEs) are commonly used as flame retardants

  • Sequencing produced approximately 48 M total reads from a blank control sample, 56 M total reads from a sample of 0.1% dimethyl sulfoxide (DMSO) vehicle, 42 M total reads from a sample of 5 μg/L BDE47, and 38 M total reads from sample of 500 μg/L BDE47

  • In general, exposure to BDE47 resulted in the body curvature phenotype and abnormal locomotion

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Summary

Introduction

Polybrominated diphenyl ethers (PBDEs) are commonly used as flame retardants. The use of commercial mixtures such as pentabromodiphenyl ether and octabromodiphenyl ether in products has been banned or limited by the European Union, the U.S, and other countries, PBDE residues in the environment and in animal tissues still pose a serious threat [1,2]. Among PBDE congeners, 2,2′,4,4′-tetrabromodiphenyl ether (CAS: 5436-43-1) is the most frequently detected one [3], and previous studies have demonstrated it to be the most toxic [4,5]. The best-known mechanism of BDE47 toxicity involves its ability to impair the homeostasis and function of thyroid hormone (TH) in animals because of its structural similarity to THs such as triiodothyronine (T3) and thyroxine (T4).

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