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The novel brominated flame retardant decabromodiphenyl ethane (DBDPE) has become a widespread environmental pollutant. However, the target tissue and toxicity of DBDPE are still not clear. In the current study, female zebrafish were exposed to 1 and 100 nM DBDPE for 28 days. Chemical analysis revealed that DBDPE tended to accumulate in the brain other than the liver and gonad. Subsequently, tandem mass tag-based quantitative proteomics and parallel reaction monitoring verification were performed to screen the differentially expressed proteins in the brain. Bioinformatics analysis revealed that DBDPE mainly affected the biological process related to muscle contraction and estrogenic response. Therefore, the neurotoxicity and reproductive disruptions were validated via multilevel toxicological endpoints. Specifically, locomotor behavioral changes proved the potency of neurotoxicity, which may be caused by disturbance of muscular proteins and calcium homeostasis; decreases of sex hormone levels and transcriptional changes of genes related to the hypothalamic-pituitary-gonad-liver axis confirmed reproductive disruptions upon DBDPE exposure. In summary, our results suggested that DBDPE primarily accumulated in the brain and evoked neurotoxicity and reproductive disruptions in female zebrafish. These findings can provide important clues for a further mechanism study and risk assessment of DBDPE.

In the current study, adult male zebrafish fed a normal diet (ND) or high-fat diet (HFD) were exposed to niclosamide (NIC) at environmentally relevant concentrations to reveal the accumulation and distribution in different tissues and evaluate the effects on liver-gut axis. Chemical analysis indicated that the liver bore a greater burden of NIC compared with the brain and gonads in adult zebrafish, and the HFD-fed fish bore greater burden in their liver and brain than those ND-fed fish. The indications from body weight, growth rate, body mass index, micro-CT images, biochemical and pathological changes confirmed that NIC can efficaciously curb weight gain and improve overloads of in plasma insulin and glucose in HFD-fed zebrafish. However, the potential effects on liver-gut axis in ND-fed zebrafish were also elucidated: NIC disturbed mitochondrial energy production, inhibited the glycemic and triacylglycerol biosynthesis but promoted triacylglycerol and free fatty acid catabolism, therefore reduced lipid accumulation in hepatocytes; NIC also impaired the physical barrier, evoked inflammatory and oxidative stress and led to microbiota dysbiosis in the intestine. There findings highlighted the necessity for evaluating its potential impacts on the health of wild animals as well as human beings upon long-term exposure.

To determine how the aryl hydrocarbon receptor (AhR) signaling acts along the gut-liver axis, we employed an integrated metagenomic and metabolomic approach to comprehensively profile the microbial and metabolic networks. Adult zebrafish were exposed to a model agonist of the AhR: polychlorinated biphenyl (PCB) 126. The metagenomic analysis showed that PCB126 suppressed microbial activities related to primary bile acid metabolism in male intestines. Accordingly, a suite of primary bile acids consistently showed higher concentrations, suggesting that bacterial conversion of primary bile acids was blocked. PCB126 also disturbed bacterial metabolism of bile acids in female intestines, as revealed by higher concentrations of primary bile acids (e.g., chenodeoxycholic acid) and activation of the nuclear farnesoid X receptor signaling. In addition, PCB126 exposure impaired the metabolism of various essential vitamins (e.g., retinol, vitamin B6, and folate). Degradation of vitamin B6 by bacterial enzymes was inhibited in male intestines, resulting in its intestinal accumulation. However, PCB126 suppressed the bacterial metabolism of vitamins in female intestines, causing systematic deficiency of essential vitamins. Overall, we found that PCB126 exposure dysregulated gut microbial activities, consequently interrupting bile acid and vitamin metabolism along the gut-liver axis. The findings provided an insight of the AhR action in microbe-host metabolic communication related to PCBs.

Due to the characteristics of persistent organic pollutants (POPs), some legacy brominated flame retardants (LBFRs) were prohibited from use, and then gradually replaced by novel brominated flame retardants (NBFRs). However, till now little research focused on the effects of NBFRs on the benthos. In the present study, 0.5, 5, and 50 mg/kg dw of pentabromotoluene (PBT), hexabromobenzene (HBB), 1,2-bis(2,4,6-tribromophenoxy) ethane (BTBPE), decabromodiphenyl ethane (DBDPE) and decabromodiphenyl ether (BDE209) were added into sediments to test freshwater clams (Corbicula fluminea). In the 35-day exposure experiment, C. fluminea had different enrichment behaviors in three treatment groups. It was conjectured that in the lower dose group, the clams ingested contaminants and tended to be stable over time. While in higher dose groups, the clams were induced by the chemicals, leading to the changes in physiological activities so that the concentrations showed a downward trend first and then went up. The half-lives of contaminants in freshwater clams were between 0.911 and 11.6 days. DBDPE showed stronger bioaccumulation ability than BDE209 in this study. Parabolic relationships were observed between log BSAF and log K

Progestins are worldwide environmental contaminants, however, their ecotoxicological risks and underlying molecular mechanisms of effects are not fully understood. In this study, newly hatched rare minnow (Gobiocypris rarus) larvae were exposed to environmentally realistic concentrations (1 and 10 ng/L) of levonorgestrel (LNG) for 6 months. The sex ratios were not affected by LNG at both concentrations, but the growth was significantly inhibited at 10 ng/L while promoted at 1 ng/L. Histological analysis revealed impaired gonadal development. Plasma concentrations of estradiol in females and testosterone in both sexes were significantly induced after exposure to 1 ng/L LNG; plasma concentrations of 11-ketotestosterone were markedly increased in females exposed to 10 ng/L LNG and in males exposed to both concentrations of LNG. The transcription of cyp19a1a was significantly up-regulated in ovaries exposed to LNG at both concentrations, while cyp17a1 was down-regulated in testes exposed to 10 ng/L LNG. The global DNA methylation level was significantly decreased in testes exposed to 10 ng/L LNG, which might be associated with inhibited spermatogenesis. Gender-specific changes in CpG methylation patterns were induced by LNG in the 5' flanking region of cyp19a1a, with hypomethylation in ovaries but hypermethylation in testes, which was linked to the regulation of cyp19a1a transcription. The results suggest that LNG could induce endocrine disrupting effects in fish at environmentally realistic concentrations, which may be linked to altered DNA methylation. This study indicates potentially high ecological risk of LNG to fish populations, and warrants researches on regulatory mechanisms of epigenetic modifications in progestin-induced effects.

Bis(2-ethylhexyl)-2,3,4,5-tetrabromophthalate (TBPH) is a ubiquitous environmental contaminant, but its toxicity is not fully understood. Accordingly, we investigated the effects of TBPH and its metabolite, mono-(2-ethyhexyl)tetrabromophthalate (TBMEHP), on lipid metabolism using a zebrafish model. The molecular docking study revealed that TBPH and TBMEHP bind to zebrafish peroxisome proliferator-activated receptor γ (PPARγ), with binding energies similar to rosiglitazone, a PPARγ agonist. Zebrafish embryos 0.75 hpf were exposed to TBPH (0.2-2000 nM) or TBMEHP (0.2-2000 nM) until 72 hpf, and their effects on PPARγ-mediated lipid metabolism were evaluated. Significant regional DNA demethylation of the PPARγ promoter was observed in the larvae at 72 hpf. Demethylation of the PPARγ promoter accompanied by upregulation of tet1 and tet2 transcription caused upregulation of PPARγ transcription and certain downstream genes involved in lipid lipolysis, transport, and metabolism. The triglyceride and total cholesterol concentrations in the larvae were significantly reduced following exposure to TBPH or TBMEHP. Furthermore, significant increases in the whole ATP content and locomotor activity in the 120 hpf larvae were observed. The overall results suggest that both TBPH and TBMEHP affect methylation of the PPARγ promoter, subsequently influencing larvae lipid metabolism via the PPARγ signaling pathway and disrupting energy homeostasis.

Nanoparticles like nano-TiO

In this study, we investigated the individual and combined effects of microplastics (MPs) and chromium (Cr) on the freshwater water flea Daphnia magna by measuring mortality, bioaccumulation, antioxidative response, multixenobiotic resistance activity, and sestrin-related mitochondrial biogenesis in short-term assays and in vivo endpoints including reproduction and adult survival rate in long-term assays. Exposure to MPs, Cr, and their combination caused significant deleterious effects and acute toxicity in D. magna. Alterations in oxidative stress occurred in the groups treated with MPs and Cr alone and together. However, upon co-exposure to MPs, the Cr concentration, measured by inductively coupled plasma optical emission spectroscopy, decreased, suggesting that MPs and Cr interact with each other. Based on enzymatic activities, we noted a decrease in MP egestion via inhibition of P-glycoprotein activity in the MP-exposed groups, and multidrug resistance-associated protein activity increased in some of the MP-exposed animals depending on Cr concentration. On the other hand, MP exposure seemed to lead to mitochondrial transcription dysfunction induced by Cr via sestrin-related mitochondrial biogenesis. Overall, these results indicate that co-exposure to MPs and Cr causes acute toxicity in D. magna but lacks the chronic toxicity (21 days) and mitochondrial dysfunction caused by Cr exposure alone.

Glyphosate (GLY) contamination widely occurred in aquatic environments including aquaculture systems and raised hazard to aquatic organisms such as fish. Probiotics have been reported to alleviate contaminants-induced toxicity. However, whether probiotics could reduce the health risk of GLY to fish remain unknown. Here we investigated the impacts of GLY on crucian carp (Carassius auratus) by focusing on the protective roles of two commonly used aquaculture probiotics, Bacillus coagulans (BC) and Clostridium butyricum (CB). Exposure to GLY significantly caused growth retardation and reduced visceral fat and intestinal lipase activity in crucian carp. 16S rRNA sequencing indicated that dysbiosis of Bacteroidetes at phylum level and Flavobacterium at genus level might be primarily responsible for GLY-induced negative growth performance. High throughput targeted quantification for metabolites revealed that GLY changed intestinal metabolites profiles, especially the reduced bile acids and short-chain fatty acids. However, the addition of BC or CB effectively attenuated the adverse effects above by remodeling the gut microbiota composition and improving microbial metabolism. The present study provides novel evidence for ameliorating the harmful effects of GLY on fish species by adding probiotics, which highlights the potential application of probiotics in reducing the health risks of GLY in aquatic environment.

Silicon dioxide nanoparticles (n-SiO

Response of terrestrial invertebrates to decabromodiphenyl ethane (DBDPE) is an emerging field of research nowadays, while cytotoxicity of DBDPE and self-defense strategies of invertebrates are poorly understood. In this study, earthworms (Eisenia fetida) were incubated in the DBDPE-spiked soil system (10, 30, 50, 70, and 100 mg kg

Cadmium (Cd), a ubiquitous environmental hazardous heavy metal, poses a significant threat to the health of aquatic organisms, including teleosts. Although the toxic profile of Cd is well recognized, little is known regarding the overall view of toxic responses to varying aquatic environmental parameters (e.g., water hardness) at an individual level. Herein, differences in water hardness were partially mimicked by adjusting Ca

Many environmental contaminants could be transmitted from parents and generate impairments to their progeny. The 2,4,6-tribromophenol (TBP), a novel brominated flame retardant which has been frequently detected in various organisms, was supposed to be bioaccumulated and intergenerational transmitted in human beings. Previous studies revealed that TBP could disrupt thyroid endocrine system in zebrafish larvae. However, there is no available data regarding the parental and transgenerational toxicity of this contaminant. Thus, in this study adult zebrafish were exposed to environmental contaminated levels of TBP for 60 days to investigate the parental and transgenerational impairments on thyroid endocrine system. Chemical analysis verified the bioaccumulation of TBP in tested organs of parents (concentration: livergonadsbrain) and its transmission into eggs. For adults, increased thyroid hormones, disturbed transcriptions of related genes and histopathological changes in thyroid follicles indicate obvious thyroid endocrine disruptions. Transgenerational effects are indicated by the increased thyroid hormones both in eggs (maternal source) and in developed larvae (newly synthesized), as well as disrupted transcriptional profiles of key genes in HPT axis. The overall results suggest that the accumulated TBP could be transmitted from parent to offspring and generate thyroid endocrine disruptions in both generations.

Bis(2-ethylhexyl)-2,3,4,5-tetrabromophthalate (TBPH), a novel brominated flame retardant, can potentially cause lipid metabolism disorder; however, its biological effects on lipid homeostasis remain unknown. We investigated its ability to cause nonalcoholic fatty liver disease (NAFLD) in zebrafish. Female zebrafish were fed a high-fat diet (HFD, 24% crude fat) or normal diet (ND, 6% crude fat), and exposed to TBPH (0.02, 2.0 μM) for 2 weeks. Consequently, HFD-fed fish showed a higher measured concentration of TBPH than ND-fed fish. Further, TBPH-treated fish in the HFD group showed higher hepatic triglyceride levels and steatosis. In comparison to ND-fed fish, treating HFD-fed fish with TBPH led to an increase in the concentration of several proinflammatory markers (e.g., TNF-α, IL-6); TBPH exposure also caused oxidative stress. In addition, the mRNA levels of genes encoding peroxisome proliferator-activated receptors were increased, and the transcription of genes involved in lipid synthesis, transport, and oxidation was upregulated in both ND- and HFD-fed fish. Both the ND and HFD groups also showed demethylation of the peroxisome proliferator-activated receptor-γ coactivator 1-α gene promoter, accompanied by the upregulation of tet1 and tet2 transcription. To summarize, we found that TBPH amplified the disruption of lipid homeostasis in zebrafish, leading to the enhancement of diet-induced NAFLD progression.

Perfluorobutanesulfonate (PFBS), an environmental pollutant of emerging concern, significantly impairs offspring development and overall health after parental exposure. However, the true inducer of offspring developmental defects among the complexity of parental influences remains unknown. In the present study, marine medaka (Oryzias melastigma) were exposed to environmentally realistic concentrations of PFBS (0, 1, 3, and 10 μg/L) for an entire life cycle. By mixing and mating control and exposed medaka (male or female), a crossbreeding strategy was employed to produce offspring eggs from various crossbreeds, with the aim of differentiating the maternal and paternal influences. Measurements of swimming performance in larval offspring showed that larvae of exposed male parents swam hyperactively in comparison to the control larvae. Contrasting trends in PFBS transfer and maternal factor transfer (e.g., proteins and lipids) to that of swimming behavior eliminated these two factors as major inducers of offspring developmental impairment. Inheritance of the exposed paternal methylome marks in offspring may be partially responsible for abnormal swimming behavior, although different toxic mechanisms may be involved depending on the exposure concentration. Overall, these findings suggest that inheritance of epigenetic modifications implicates a long-lasting threat of PFBS to the fitness and sustainability of fish populations.

Synthetic pyrethroids (SPs) are broadly used to control pests and have been widely detected in aquatic environments, prompting concern over its risk to the health of non-target organisms. The present study evaluated whether long-term (60 d) exposure to low doses (0, 20, 100, and 500 ng/L) of cis-BF enantiomers (1S-cis-BF and 1R-cis-BF) could cause reproductive endocrine disturbance to zebrafish. Exposure to 1S-cis-BF has stronger reproductive impairment effect than 1R-enantiomer, indicating that the enantioselectivity of cis-BF on fish reproduction. Significant decrease of cumulative spawning of zebrafish was observed as a result of cis-BF exposure. And the retardations of testis and ovaries development found in histopathological section were suggested to be important cause for the decreased fecundity. Cis-BF decreased the total motility of sperm but did not affect sperm density. Relatively high levels of cis-BF detected in the gonads of males and females may directly impair gametogenesis. In addition, alterations in the expression of key genes (cyp17, cyp19a and 17β-hsd) associated with reproductive endocrine pathways were correlated well with the significant changes in sex hormone contents (E2 and T) and these results may relate to gonadal development and maturation of germ cells in females or/and males which were suspected to be a likely underlying mechanism. Furthermore, the reduction of quality of F1 embryo derived from the unexposed females and exposed males (UE♀ × E♂) demonstrated that male exposure had greater adverse effects on offspring. Our results indicate that long term, low dose exposure to cis-BF can enantioselectively impair the reproduction system of fish, and induce toxicity related abnormalities in non-exposed offspring. This study has important implications for environmental risk assessment of chiral pesticides that are concurrently present in aquatic systems.

Perfluorobutanesulfonate (PFBS) is increasingly polluting aquatic environments due to worldwide manufacturing and application. However, toxicological knowledge regarding PFBS exposure remains scarce. Here, we showed that PFBS life-cycle exposure at environmentally realistic concentrations (0, 1.0, 2.9, and 9.5 μg/L) skewed the sex ratio in fish toward male dominance, while reproductive functions of female fish were greatly impaired, as characterized by extremely small ovaries, blocked oocyte development, and decreased egg production. Endocrine disruption through the hypothalamus-pituitary-gonad axis was induced by PFBS exposure, showing antiestrogenic activity in females but estrogenic activity in males. PFBS was found to gradually accumulate in F0 adults during continuous exposure but can be rapidly eliminated when depurated in clean water. Parental exposure also transferred PFBS pollutant to F1 offspring eggs. Although no trace of PFBS was detected in F1 adults and F2 eggs, adverse effects from parental exposure persisted in F1 and F2 offspring. These transgenerational effects implicate PFBS as an ongoing threat to the fitness and sustainability of fish populations. The dramatic impairment of fish reproduction highlights the urgency of re-evaluations of the ecological and evolutionary consequences of PFBS exposure.

The photolysis of four typical NBFRs decabromodiphenyl ethane (DBDPE), bis(2-ethylhexyl) tetrabromophthalate (TBPH), pentabromotoluene (PBT) and hexabromobenzene (HBB) were first explored under different sources of light, two temperatures, organic solvents and the presence of humic substance (HS). Degradation could be described by pseudo-first-order kinetic model. Under different irradiation sources, the degradation rates were in order of UVC (0.0616-0.137 min(-1)) > UVB (0.0348-0.0810 min(-1)) > sunlight (0.0102-0.0370 min(-1)) > UVA (almost no degradation). Under UVB irradiation, the half-life of NBFRs was the lowest in tetrahydrofuran (6.16-22.77 min), and the longest (93.42- > 120 min) in acetone, indicating that organic solvents greatly affected the degradation kinetics. HS could influence the degradation, and DBDPE or TBPH respectively declined 13.92-30.68% and 12.17-59.41% at 240 min, while the degradation of PBT and HBB were highly inhibited. TBPH photolysis was affected by humic acid (HA) or fulvic acid (FA) concentration, but DBDPE degradation barely showed significant difference (p < 0.05) in the presence of 1 and 10 mg L-1 of HA. Photolytic products of the four NBFRs were identified by GC-NCI/EI-MS, indicating that the photodegradation process was mainly stepwise debromination from high-down to low-bromine-substituted NBFRs. 2,4,6-triBT and 2,4,5-triBT were identified as products of PBT. PBB, 1,2,4,5-tetraBB, 1,2,4-triBB, 1,3,5-triBB and 1,3/1,2-diBB were identified as products of HBB. Our observations could provide a few insights into the removal of NBFRs in a liquid environment.

Contamination of perfluoroalkyl acids (PFAAs) is ubiquitously detected in various environments. However, their potential effects on microbial communities remain largely unknown. In this study, surface seawater of the Pearl River Delta (PRD) is sampled to measure PFAA concentrations and profile the structure of free-living microbial community. Total PFAAs concentrations range from 131 to 1563 pg L−1 in surface seawater. PFOS (16–470 pg L−1), PFOA (27–272 pg L−1), PFHpA (18–201 pg L−1) and PFBA (25–152 pg L−1) are the major homologues, indicating continued industrial application or release of PFOS and a gradual shift towards using shorter-chain PFAAs. Concentrations of PFAAs from this recent cruise are much lower than previous reports, which may be due to the effective management of PFAA usage around PRD region. In addition, the microbial community in PRD surface seawater is predominantly colonized by the Proteobacteria phylum (27.2 to 61.5%) and the Synechococcus genus (5.6 to 38.6%). The structure of the microbial communities varies among stations, mainly resulting from different abundances of Synechococcus, Prochlorococcus and Nitrosopumilus. Geochemical parameters (e.g., nutrients and salinity) and phytoplankton are significantly associated with the microbial community dynamics in surface seawater. In the interactive network of microbiota, a subset of bacteria (i.e., Fluviicola, Nitrosopumilus, Limnohabitans, Sediminibacterium, C39 and Polynucleobacter) shows significantly positive correlations with PFAAs (R > 0.6; P

Environmental microbiota play essential roles in the maintenance of many biogeochemical processes, including nutrient cycling and pollutant degradation. They are also highly susceptible to changes in environmental stressors, with environmental pollutants being key disruptors of microbial dynamics. In the present study, a scientific cruise was launched on July 2017 around Pearl River Delta, a suitable studying site for perfluoroalkyl substances (PFASs) in the wake of the severe PFAS pollution. Surface sediment samples were collected from 18 representative stations to assess PFAS accumulation and profile microbial community. PFAS concentrations ranged from 24.2 to 181.4 pg/g dry weight in sediment, and perfluorooctanesulfonic acid (PFOS) was the dominant homologue. The concentrations of PFAS homologues in the current study were much lower than those reported in previous studies, implying effective management and control of pollution from PFAS-related industries. 16S rRNA gene amplicon sequencing revealed that Proteobacteria was the dominant phylum, while nitrogen-metabolizing Nitrosopumilus and sulfate-reducing Desulfococcus genera were the most abundant. Variations in microbial communities among sampling stations were mainly due to the differences in abundances of Escherichia, Nitrosopumilus, and Desulfococcus. The outbreak of Escherichia bacteria at specific coastal stations potentially indicated the discharge of fecal matter into the marine environment. Dissolved oxygen (DO) in bottom seawater significantly influenced the structure of microbial communities in the sediment, while current study failed to observe significant effects from PFAS pollutants. Positive correlations were found between DO and sulfate-reducing bacteria in Desulfococcus and GOUTA19 genera. Overall, this study explored relationships between environmental variables (e.g., PFAS pollutants) and sediment bacteria. Biogeochemical parameters significantly influenced the structure and composition of microbial communities in sediment.

Titanium dioxide (TiO2) nanoparticles and bisphenol A (BPA) in aquatic environments interact reciprocally to enhance the maternal transfer of pollutants to offspring, thus varying the innate toxicities during early embryonic development. However, it remains unexplored regarding the molecular mechanisms of developmental toxicity in offspring after parental coexposure. In the present study, adult zebrafish were exposed to TiO2 nanoparticles (100 mu g/L), BPA (20 mu g/L) or their binary mixture for four months. Then, eggs of F1 generation were collected and reared in clean water until 5 days post-fertilization. In characteristic of larval survival and growth, parental coexposure to TiO2 particles and BPA caused a severer inhibition of F1 offspring larvae compared with single exposure. Mechanistic investigation by shotgun proteomics found that development of larval offspring from coexposed parents was impaired through a distinct mode of toxicity, that is, specifically altering the activity of phagosome and lysosome. Single exposure of adult zebrafish to TiO2 mainly affected insulin-responsive compartment; and BPA parental exposure mainly affected carbohydrate metabolism and calcium signaling of larval offspring. Furthermore, considering the tight regulation of sex hormones in the expression of vitellogenin (VTG), addition of nanoparticles during parental exposure led to inconsistencies between VTG induction and endogenous levels of sex hormones (estradiol and testosterone) in F1 offspring fish. This implied that transfer of nanoparticles to offspring larvae may change the availability of hormonal molecules and BPA at target tissues. Overall, current results provided mechanistic clues into the multigenerational developmental toxicity by parental coexposure to TiO2 particles and BPA. (C) 2018 Elsevier Ltd. All rights reserved.

The coexistence of organic toxicants and nanoparticles in the environment influences pollutant bioavailability and toxicity. Using chronic co-exposure to an adult zebrafish model, this study investigated the transfer kinetics and transgenerational effects of bisphenol A (BPA) and titanium dioxide nanoparticles (n-TiO2) exposure in F1 offspring. When single and combined exposure to BPA (0, 2, and 20 μg/L) and n-TiO2 (100 μg/L) were compared, combined exposure was found to reciprocally facilitate bioaccumulation in adult fish while enhancing maternal transfer to offspring. Thyroid endocrine disruption and developmental neurotoxicity were observed in larval offspring by parental exposure to BPA alone or in combination with n-TiO2. Exposure to 20 μg/L BPA significantly decreased the thyroxine (T4) concentration in adult plasma, leading to less transfer into the eggs. The presence of 20 μg/L BPA with n-TiO2 further decreased the level of T4 compared to BPA exposure alone. Additionally, offspring larvae derived from exposed parents exhibited lethargic swimming behavior. Overall, this study examined the interactions of BPA and n-TiO2 with regard to their bioaccumulation, maternal transfer, and developmental effects, which highlighted that co-exposure dynamics are important and need to be considered for accurate environmental risk assessment.

Our study evaluated the current occurrence, composition, and spatial distribution of eight congeners of polybrominated diphenyl ethers (PBDEs) and seven novel brominated flame retardants (NBFRs) in sediment from Guiyu, a typical e-waste dismantling region in China. PBDEs levels ranged from 0.345 to 401,000 ng/g dw and NBFRs levels ranged from 0.581 to 73,100 ng/g dw. Almost all sediment samples contained high levels of BDE-209 and DBDPE, and the ratio of DBDPE/BDE-209 in sediments ranged from 0.0814 to 2.80 (mean: 0.879). The concentration and composition profiles for BFRs in sediments from both mainstream and tributaries of two major rivers in Guiyu reach (and adjacent downstream locations) differed significantly from those far from Guiyu town. Whereas the high presence of BFRs in Guiyu reflected the historical crude e-waste dismantling activities in the region; the locations far from Guiyu town were likely to receive BFRs from atmospheric deposition, not originated from the region, as BFRs in water-sediment are known to be able to migrate a limited distance along the river. Ecological risk assessment revealed that the low brominated congeners of PBDEs and BDE-209 posed an unacceptable risk to the sedimentary life at multiple locations. Our results updated our knowledge of BFRs contamination in Guiyu, suggesting the necessity of continuous source monitoring, control procedures, and sediment cleanup for BFRs.

Deltamethrin, a widely used type II pyrethroid insecticide, was reported with neurotoxicity to aquatic organisms, such as fish. However, the effects and potential mechanisms on the central nervous system remain largely unknown, especially under environmental concentrations. Therefore, we exposed adult female zebrafish to environmentally relevant levels of deltamethrin (30, 100, and 333 ng/L) for 21 days to assess neurobehavioral changes related to the central nervous system and explore the modes of action. Behavioral assays revealed significant increases in the swimming speeds, residence time near other fish and the shoaling cohesion in exposed fish. Transcriptomic results enriched the disrupted neural functions involving the glutamatergic and dopaminergic synapses in the brain. The qRT-PCR confirmed the upregulation of the factors for promoting the glutamate release. The measurement of neurotransmitters showed significantly increased content of the excitatory neurotransmitter glutamate in the brain. Taken together, deltamethrin exposure increased the glutamate level and promoted the release of such an excitatory neurotransmitter between the glutamatergic synapses in the brain, which eventually led to hyperactivity of social behaviors in adult zebrafish.

Synthetic progestins are widely used pharmaceutical agents that have become common contaminants in the aquatic environment. The potential adverse effects of long-term exposure on aquatic wildlife, however, are not fully understood. The aim of this study was to investigate the endocrine disruption in Chinese rare minnow (Gobiocypris rarus) in response to megestrol acetate (MTA) exposure. Newly-hatched Chinese rare minnow larvae were exposed to MTA at a nominal concentration of either 1 ng/L (detected concentrations ranged from 0.18 to 0.93 ng/L) or 10 ng/L (detected concentrations ranged from 4.27 to 9.64 ng/L) for 6 months and the effects on growth, sex steroid hormones, gonadal histology, and steroidogenic genes expression were determined. After 6 months of exposure to a nominal concentration of 10 ng/L MTA, the body weight and condition factors were significantly increased in fish of both sexes. Exposure to a nominal concentration of 10 ng/L MTA significantly reduced plasma concentrations of estradiol and 11-ketotestosterone in female fish while also reducing testosterone and 11-ketotestosterone in male fish. Gonad histology revealed significantly reduced proportions of vitellogenic oocytes in female fish exposed to a nominal concentration of 10 ng/L MTA and induction of atretic follicles in female fish exposed to both nominal concentrations of MTA. The expression of cyp19a1a and cyp17a1 in the gonads was up-regulated in the ovaries while down-regulated in the testes. Our results indicate that MTA can induce endocrine disruption in Chinese rare minnow at the low concentrations found in contaminated environments. This indicates a potentially high ecological risk from MTA to fish populations in MTA-contaminated aquatic environments in China and may also in other regions.

As the two most commonly used organophosphorus herbicides, glyphosate (Gly) and glufosinate-ammonium (Glu) have unique properties for weed control and algae removal in aquaculture. However, the occurrences and health risks of Gly and Glu in aquaculture ponds are rare known. This study aimed to investigate the occurrences of Gly, AMPA (primary metabolity of Gly) and Glu in surface water, sediment and aquatic products from the grass carp (ctenopharyngodon idella), crayfish (procambarus clarkii) and crab (eriocheir sinensis) ponds around Lake Honghu, the largest freshwater lake in Hubei province, China where aquaculture has become the local pillar industry. Three age groups (children, young adults, middle-aged and elderly) exposure to these compounds through edible aquatic products (muscle) consumption were also assessed by target hazard quotient (THQ) method. The results indicated that Gly, AMPA and Glu were widely occurred in surface water, sediment and organisms in the fish, crayfish and crab ponds. AMPA was more likely to accumulate in the intestine of aquatic products than Gly and Glu. According to the total THQ value (1.04＞1), muscle consumption of grass carp may pose potential risk to children.

Bis(2ethylhexyl)-2,3,4,5-tetrabromophthalate (TBPH), a replacement for restricted flame retardants, has become ubiquitous in the environment. To reveal the neurotoxicity and underlying mechanism of TBPH, we first evaluated its penetrability through the blood-brain barrier (BBB) using hCMEC/D3 cells as in vitro model, and found TBPH had poor penetrability through BBB with a maximum Papp of 14.8 × 10−6 cm s−1. Further study using transgenetic zebrafish (Tg flk1: EGFP) as in vivo model confirmed that TBPH could affect the BBB permeability, probably via affecting the transcription of genes encoding tight junction proteins. Finally, wild type zebrafish embryos/larvae were exposed to TBPH to evaluate the neurotoxicity. The neurodevelopment, neurotransmitters and locomotor activity of zebrafish larvae did not changed, which may be because TBPH can hardly cross the BBB to pose direct exposure to the central nervous system. However, the transcription of opsins genes and visual response to light stimulation in zebrafish larvae were inhibited, pointing to additional mechanism that may cause visual impairment indirectly. Above all, these results can help further understand the neurotoxicity and underlying mechanism by TBPH, and also pointed out potential risk of this chemical to aquatic organisms.

Tris (1,3-dichloro-2-propyl) phosphate (TDCIPP), an alternative to brominated flame retardants, might pose an exposure risk to humans and wild animals during fetal development. Our recent study suggested that short-term TDCIPP exposure during early development caused sex-dependent behavioral alteration in adults. In the present study, multigenerational neurodevelopmental toxicity upon early-life exposure of parental zebrafish was evaluated, and the possible underlying mechanisms were further explored. Specifically, after embryonic exposure (0–10 days post-fertilization, dpf) to TDCIPP (0, 0.01, 0.10, and 1.00 μM), zebrafish larvae were cultured in clean water until the sexually matured to produce progeny (F1). The results confirmed neurodevelopmental toxicity in F1 larvae characterized by changes of developmental endpoints, reduced thigmotaxis, as well as altered transcription of genes including myelin basic protein a (mbpa), growth associated protein (gap43) and synapsin IIa (syn2a). Sex-specific changes in thyroid hormones (THs) indicated the relationship of abnormal THs levels with previously reported neurotoxicity in adult females after early-life exposure to TDCIPP. Similar changing profiles of TH levels (increased T3 and decreased T4) in adult females and F1 eggs, but not in F1 larvae, suggested that the TH disruptions were primarily inherited from the maternal fish. Further results demonstrated hypermethylation of global DNA and key genes related to TH transport including transthyretin (ttr) and solute carrier family 16 member 2 (slc16a2), which might affect the transport of THs to target tissues, thus at least partially contributing to the neurodevelopmental toxicity in F1 larvae. Overall, our results confirmed that early-life TDCIPP exposure of parental fish could affect the early neurodevelopment of F1 offspring. The underlying mechanism could involve altered TH levels inherited from maternal zebrafish and epigenetic modifications in F1 larvae.

The flame retardants hexabromobenzene (HBB) and pentabromobenzene (PBB) have been extensively used and become ubiquitous pollutants in the aquatic environment and biota, but their potential toxic effects on wildlife remained unknown. In this study, by using zebrafish (Danio rerio) as a model, the bioconcentration and developmental neurotoxicity were investigated. Zebrafish embryos were exposed to HBB and PBB (0, 30, 100 and 300 μg/L) from 2 until 144 h post-fertilization (hpf). Chemical analysis showed bioconcentrations of both chemicals, while HBB is readily metabolized to PBB in zebrafish larvae. Embryonic exposure to both chemicals did not cause developmental toxicity, but induced locomotor behavioral anomalies in larvae. Molecular docking results indicated that both chemicals could bind to zebrafish acetylcholinesterase (AChE). Furthermore, HBB and PBB significantly inhibited AChE activities, accompanied by increased contents of acetylcholine and decreased choline in larvae. Downregulation of the genes associated with central nervous system (CNS) development (e.g., mbp, α1-tubulin, gfap, shha) as well as the corresponding proteins (e.g., Mbp, α1-Tubulin) was observed, but gap-43 was upregulated at both gene and protein levels. Together, our results indicate that both HBB and PBB exhibit developmental neurotoxicity by affecting various parameters related to CNS development and indications for future toxicological research and risk assessment of the novel brominated flame retardants.

To determine whether and how probiotic supplement can alter gut microbiota dysbiosis and lipid metabolism disorders caused by perfluorobutanesulfonate (PFBS), the present study exposed adult zebrafish to 0, 10, and 100 μg/L PFBS for 28 days, with or without dietary administration of probiotic Lactobacillus rhamnosus. Regarding intestinal health and gut microbiota, probiotic supplement altered the innate toxicities of PFBS, depending on exposure concentration and the sex of the fish. Lactobacillus genus correlated positively (P 0.5) with other beneficial bacteria in the gut microbiota, thereby indirectly regulating host metabolic activities. In female fish, the PFBS and probiotic combination enhanced fatty acid synthesis and β-oxidation, but mitigated the accumulation of cholesterol in the blood compared with PFBS single exposure, highlighting the benefits of the probiotic to host health. In male zebrafish, probiotic administration antagonized the PFBS-induced disturbances of bile acid metabolism, presumably via farnesoid X receptor signaling. However, coexposure to PFBS and probiotic caused significant accumulation of triglyceride in male livers (2.6-fold relative to the control), implying the induction of hepatic steatosis. Overall, the present study underlined the potential of probiotics to modulate gut microbial dysbiosis and lipid metabolism disorders caused by PFBS exposure, which could provide implications to the application of probiotics in aquaculture.

The present study exposed adult zebrafish to 0, 10, and 100 μg/L perfluorobutanesulfonate (PFBS) with or without dietary supplement of probiotic Lactobacillus rhamnosus. Interaction between probiotic and PFBS on sex endocrine and reproduction was investigated. It was striking to find that PFBS and probiotic coexposures almost ceased the fecundity, which was accompanied by disturbances in sex hormones and oocyte maturation in females. In contrast, probiotic additive efficiently antagonized the estrogenic activity of PFBS in males. For the first time, this study reported that probiotic heavily depended on sex to modulate the endocrine disruption and reproductive toxicity of aquatic pollutants.

Parental exposure to perfluorobutane sulfonate (PFBS), an aquatic pollutant of emerging concern, is previously found to impair the embryonic development of offspring. However, the impairing mechanisms remain to clarify. In the present study, adult zebrafish were exposed to 0, 10 and 100 μg/L PFBS for 28 d, after which disturbances in maternal transcript transfer and offspring embryogenesis were investigated. Prior to zygotic genome activation, high-throughput transcriptomic sequencing revealed that parental PFBS exposure significantly altered the transcript profile of maternal origin in offspring eggs, while toxic actions varied as a function of PFBS concentrations. In offspring eggs derived from 10 μg/L exposure group, differential transcripts were mainly associated with the histone-DNA interaction of nucleosome, which would modify the compacted chromatin configuration and accessibility of transcriptional factors to DNA sequences. In this regard, the timing of zygotic genome activation was presumably disrupted. Parental exposure to 100 μg/L PFBS primarily interrupted the maternal transfer of adherens junction transcripts, which was supposed to dysregulate the cell-cell adhesion during early embryo formation. Development and growth of offspring embryos were significantly compromised by parental PFBS exposure, as exemplified by higher mortality, delayed hatching, slower heart rate, reduced body weight and neurobehavioral disorders. Overall, the present study presented the first toxicological evidence about the disturbances of PFBS in maternal transcript transfer, although the inherent linkage between maternal transcript modifications and offspring development defects still needs future works to construct.

Perfluorobutane sulfonate (PFBS), an environmental pollutant of emerging concern, is previously shown to dynamically interact with hypoxia on aquatic developmental toxicities. However, the molecular mechanisms underlying the interaction remain unknown. In this follow-up study, marine medaka embryos were exposed to 0 and 3.3 mg/L of PFBS under normoxia (6.9 mg/L) or hypoxia (1.7 mg/L) condition till 15 days post-fertilization. High-throughput transcriptomic sequencing was employed to filter differentially expressed genes and provide mechanistic insight into interactive action between hypoxia and PFBS. The results showed that hypoxia alone and the coexposure paradigm were similarly potent to modify transcriptional profiles, with the majority of genes significantly down-regulated. In contrast, transcriptional toxicity of PFBS was relatively milder. Functional annotation analyses found that hypoxia and coexposure groups mainly impacted phototransduction signaling by decreasing the transcriptions of cyclic nucleotide-gated (CNG) cation channels and retinol transport genes. However, this study demonstrated the first toxicological evidence that toxic effects of PFBS targeted the perception of chemical stimulus through olfactory and gustatory receptors. The addition of PFBS moderately exacerbated the toxic actions of hypoxia, which largely shaped the transcriptional pattern of coexposure group. In addition, gene interactive networks were constructed for hypoxia and coexposure groups, underlining the increased chromatin deacetylation and methylation to epigenetically repress genome-wide transcriptional initiation. Overall, PFBS and hypoxia interact to interrupt the embryonic development of sensory systems, which may compromise the individual fitness and survival, especially during early life stages when precocious perception of food and escape from predators are essential.