Parental exposure to polybrominated diphenyl ethers (PBDEs) in animals has been found to be transferred to the offspring. The environmental health risk and toxicity to the offspring are still unclear. The objective of the present study was to identify environmentally relevant concentrations of PBDEs for parental exposure that would cause developmental neurotoxicity in the offspring. Adult zebrafish were exposed to environmentally relevant concentrations of 0.8, 4.0 μg/L) via water. The results showed that PBDE exposure did not affect larvae hatching, malformation, or survival. The residue of PBDEs was detected in F1 eggs upon parental exposure. Acetylcholinesterase (AChE) activity was significantly inhibited in F1 larvae. Genes of central nervous system development (e.g., myelin basic protein, synapsin IIa, α1-tubulin) were significantly downregulated in larvae. Protein levels of α1-tubulin and synapsin IIa were also reduced. Decreased locomotion activity was observed in the larvae. This study provides the first evidence that parental exposure to environmentally relevant concentrations of PBDEs could cause adverse effects on neurodevelopment in zebrafish offspring.

No abstract

Various antifouling (AF) coatings have been developed to protect submerged surfaces by deterring the settlement of the colonizing stages of fouling organisms. A review of the literature shows that effective AF compounds with specific targets are ones often considered non-toxic. Such compounds act variously on ion channels, quorum sensing systems, neurotransmitters, production/release of adhesive, and specific enzymes that regulate energy production or primary metabolism. In contrast, AF compounds with general targets may or may not act through toxic mechanisms. These compounds affect a variety of biological activities including algal photosynthesis, energy production, stress responses, genotoxic damage, immunosuppressed protein expression, oxidation, neurotransmission, surface chemistry, the formation of biofilms, and adhesive production/release. Among all the targets, adhesive production/release is the most common, possibly due to a more extensive research effort in this area. Overall, the specific molecular targets and the molecular mechanisms of most AF compounds have not been identified. Thus, the information available is insufficient to draw firm conclusions about the types of molecular targets to be used as sensitive biomarkers for future design and screening of compounds with AF potential. In this review, the relevant advantages and disadvantages of the molecular tools available for studying the molecular targets of AF compounds are highlighted briefly and the molecular mechanisms of the AF compounds, which are largely a source of speculation in the literature, are discussed.

The brominated flame retardant decabromodiphenyl ethane (DBDPE), an alternative to decabrominated diphenyl ether (BDE209), has become a widespread environmental contaminant, but its possible toxic effects to wildlife remain unknown. Using zebrafish as a model, we investigated the bioconcentration and impact of DBDPE on thyroid endocrine function after water-borne exposure, compared to BDE209. Zebrafish embryos were exposed to DBDPE or BDE209 (0, 3, 10, 30, 100, 300 nM) for 6 or 14 days. Chemical analysis revealed that DBDPE and BDE209 were bioconcentrated in zebrafish larvae, with similar magnitudes of accumulated concentrations. Based on screened by chromatograms, at least seven unknown compounds were observed in DBDPE-treated larvae, indicating biotransformation of the chemical. Significant increases in whole body content of triiodothyronine (T3) and thyroxine (T4) were detected in DBDPE-treated larvae, but decreased in BDE209-treated groups. Alterations in gene transcription along the related hypothalamic-pituitary-thyroid (HPT) axis were observed. Furthermore, the binding and transport protein transthyretin (TTR) was significantly increased in DBDPE exposure groups. Histological examination and stereological analysis showed no obvious pathological changes in the thyroid gland. The present study demonstrates for the first time the bioavailability, biotransformation and thyroid endocrine disruption associated with DBDPE exposure in fish. Further studies are warranted to identify the metabolites of DBDPE and to define its environmental risks to aquatic organisms.

Accumulation of perfluorobutanesulfonate (PFBS) is frequently detected in biota, raising concerns about its ecological safety. However, hazardous effects of PFBS remain largely unexplored, especially for endocrine disrupting potency. In the present study, the multigenerational endocrine disrupting potential of PFBS was investigated by exposing F0 marine medaka eggs to PFBS at different concentrations (0, 1.0, 2.9, and 9.5 μg/L) until sexual maturity. The F1 and F2 generations were reared without continued exposure. Thyroidal disturbances were examined in all three generations. PFBS exposure decreased the levels of 3,5,3'-triiodothyronine (T3) in F0 female blood; however, it increased T3 or thyroxine (T4) levels in F0 brains, in which hyperthyroidism suppressed the local transcription of 5'-deiodinase 2 ( Dio2). Obviously decreased T3 was transferred to F1 eggs, although the parental influences were reversed in F1 larvae. Delayed hatching was coupled with elevated T3 levels in F1 larvae. F1 adults showed comparable symptoms of thyroidal disruption with F0 adults. A slight recovery was noted in the F2 generation, although F2 larvae still exhibited thyroid disruption and synthesized excessive T4. Our results suggested that the offspring suffered more severe dysfunction of the thyroidal axis albeit without direct exposure. This study provided the first molecular insight about PFBS toxicology on the thyroid, beneficial to both human and environmental risk assessment.

No abstract

To determine how environmental pollutants induce dysbiosis of the gut microbiota, we exposed adult zebrafish to model pollutants with varied modes of action (atrazine, estradiol, polychlorinated biphenyl [PCB]126, and PCB153) for 7 days. Subsequently, metagenomic sequencing of the intestines was performed to compare the gut microbiomes among the groups. We observed clear compound- and sex-specific responses to xenobiotic stress. Principal component analysis revealed involvement of the aryl hydrocarbon receptor (AhR) and, to a lesser extent, the estrogen receptor (ER) in the dysregulation of the intestinal microbiota. The model pollutants differentially impaired intestinal and hepatic physiological activities, as indicated by assessments of gut motility, epithelial permeability, inflammation, and oxidative stress. Correlation analysis showed that abnormal Aeromonas reproduction, especially in the PCB126 groups, was significantly positively associated with oxidative damage. Aeromonas closely interacted with Mannheimia and Blastococcus to regulate intestinal permeability. In summary, we demonstrated that ER and AhR signaling regulated the dynamics of the gut microbiota. Our findings provide new mechanistic insight into the complex interactions between the host metabolism and gut microbiota, which may contribute to the grouped assessment of environmental pollutants in future.

In this study, marine medaka (Oryzias melastigma) were chronically exposed for 28 days to environmentally realistic concentrations of 4,5-dichloro-2-n-octyl-4-isothiazolin-3-one (DCOIT) (0, 0.76, 2.45, and 9.86 μg/L), the active ingredient in commercial antifouling agent SeaNine 211. Alterations of the hypothalamus-pituitary–gonadal-liver (HPGL) axis were investigated across diverse levels of biological organization to reveal the underlying mechanisms of its endocrine disruptive effects. Gene transcription analysis showed that DCOIT had positive regulatory effects mainly in male HPGL axis with lesser extent in females. The stimulated steroidogenic activities resulted in increased concentrations of steroid hormones, including estradiol (E2), testosterone (T), and 11-KT-testosterone (11-KT), in the plasma of both sexes, leading to an imbalance in hormone homeostasis and increased E2/T ratio. The relatively estrogenic intracellular environment in both sexes induced the hepatic synthesis and increased the liver and plasma content of vitellogenin (VTG) or choriogenin. Furthermore, parental exposure to DCOIT transgenerationally impaired the viability of offspring, as supported by a decrease in hatching and swimming activity. Overall, the present results elucidated the estrogenic mechanisms along HPGL axis for the endocrine disruptive effects of DCOIT. The reproductive impairments of DCOIT at environmentally realistic concentrations highlights the need for more comprehensive investigations of its potential ecological risks.