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Perfluorooctane sulfonate (PFOS), one persistent organic pollutant, has been widely detected in the environment, wildlife and human. Currently few studies have documented the effects of chronic PFOS exposure on lipid metabolism, especially in aquatic organisms. The underlying mechanisms of hepatotoxicity induced by chronic PFOS exposure are still largely unknown. The present study defined the effects of chronic exposure to low level of PFOS on lipid metabolism using zebrafish as a model system. Our findings revealed a severe hepatic steatosis in the liver of males treated with 0.5μM PFOS as evidenced by hepatosomatic index, histological assessment and liver lipid profiles. Quantitative PCR assay further indicated that PFOS significantly increase the transcriptional expression of nuclear receptors (nr1h3, rara, rxrgb, nr1l2) and the genes associated with fatty acid oxidation (acox1, acadm, cpt1a). In addition, chronic PFOS exposure significantly decreased liver ATP content and serum level of VLDL/LDL lipoprotein in males. Taken together, these findings suggest that chronic PFOS exposure induces hepatic steatosis in zebrafish via disturbing lipid biosynthesis, fatty acid β-oxidation and excretion of VLDL/LDL lipoprotein, and also demonstrate the validity of using zebrafish as an alternative model for PFOS chronic toxicity screening.

As a persistent organic contaminant, perfluorooctanesulphonic acid (PFOS) has been widely detected in the environment, wildlife, and humans. The present study revealed that zebrafish embryos exposed to 16 µM PFOS during a sensitive window of 48–96 hour post-fertilization (hpf) disrupted larval morphology at 120 hpf. Malformed zebrafish larvae were characterized by uninflated swim bladder, less developed gut, and curved spine. Histological and ultrastructural examination of PFOS-exposed larvae showed structural alterations in swim bladder and gut. Whole genome microarray was used to identify the early transcripts dysregulated following exposure to 16 µM PFOS at 96 hpf. In total, 1,278 transcripts were significantly misexpressed (p < 0.05) and 211 genes were changed at least two-fold upon PFOS exposure in comparison to the vehicle exposed control group. A PFOS-induced network of perturbed transcripts relating to swim bladder and gut development revealed that misexpression of genes were involved in organogenesis. Taken together, early life stage exposure to PFOS perturbs various molecular pathways potentially resulting in observed defects in swim bladder and gut development.

Bisphenol A (BPA) is a ubiquitous contaminant in environment and human body. The reproductive and developmental effects of BPA exposure in aquatic and laboratory animals have been extensively studied. However, BPA exposure on the nervous system and motor behavior development are not well understood. In this study, we utilized zebrafish embryo as a model system to investigate the effect of developmental BPA exposure on larval teratology, motor behaviors, axonal growth of spinal motoneurons and muscle structure at various developmental stages. Our findings revealed that BPA exposure altered spontaneous movement, significantly decreased touch response and swimming speed in response to light stimulation in developing zebrafish. These effects were observed at the concentrations that did not yield any significant teratogenic effects. Correlated with those changes in swimming activity, BPA-induced axial muscle damage occurred at the same concentration range (1-15 μM), but disruption of axonal growth of primary and secondary motoneuron occurred only at higher concentration (15 μM). BPA-induced apoptotic cell death subsequent to initial ROS formation and oxidative DNA damage may be the underlying mechanism for axial muscle damage, suggesting the functional relevance of muscle structural changes and the observed deficits in swimming activity.

Polybrominated diphenyl ethers (PBDEs) are ubiquitous environmental pollutants detected in a wide variety of environmental matrixes and pose a significant public health concern. 2,2',4,4'-Tetrabromodiphenyl ether (BDE-47) is one of the most predominant PBDE congeners in environmental media, biota and human tissues. However, few studies have explored the BDE-47 developmental neurotoxicity and underlying mechanisms. In this study, zebrafish (Danio rerio) embryos were waterborne exposed to BDE-47 at 1.25, 5, 20 μM starting from 6h post-fertilization (hpf). Motor behavior development and swimming behavior in response to light-to-dark photoperiod stimulation were studied at various developmental stages. Our data indicate that BDE-47 exposure significantly affected spontaneous movement, decreased touch response and free swimming speed, altered larvae swimming behavior in response to light stimulation in developing zebrafish. Consistent with these motor deficits, BDE-47 significantly inhibited axonal growth of primary and secondary motor neurons during the early developmental stages, suggesting the functional relevance of structural changes. Our findings demonstrate that the altered patterns of neuronal connectivity may contribute to motor behavior deficits, indicating the relevance of zebrafish as a model for studying toxicant developmental neurotoxicity.

Polybrominated diphenyl ethers (PBDEs) have been used extensively in electrical and electronic products, but little is known about the exposure level in the electrical appliance factories workers and nearby local residents. In this study, we assessed body burdens of PBDEs in 194 Chinese injection workers from electrical appliance factories and also measured 205 blood samples from catering workers, leather factory workers, umbilical cord and infertile men for comparison. Twelve PBDE congeners in serum samples were measured by GC–MS. The highest concentration for total PBDEs was found in injection workers, which is positively correlated to employment duration. BDE-209 was the most dominant congener followed by BDE-47, 28 and 99. We also found the presence of all twelve PBDEs in cord blood, suggesting an evidence of fetal exposure. Concentration of BDE-47 was particularly higher in serum samples from infertile men in comparison with that of catering workers and leather factory workers.