Isothiazolinone Disrupts Reproductive Endocrinology by Targeting the G-Protein-Coupled Receptor Signaling.

The unintended exposure of humans and animals to isothiazolinones has led to an increasing concern regarding their health hazards. Isothiazolinones were previously found to disrupt reproductive endocrine homeostasis. However, the long-term reproductive toxicity and underlying mechanism remain unclear. In this study, life-cycle exposure of medaka to dichlorocthylisothiazolinone (DCOIT), a representative isothiazolinone, significantly stimulated the gonadotropin releasing hormone receptor (GnRHR)-mediated synthesis of follicle stimulating hormone and luteinizing hormone in the brain. Chem-Seq and proteome analyses revealed disturbances in the G-protein-coupled receptor, MAPK, and Ca2+ signaling cascades by DCOIT. The G protein αi subunit was identified as the binding target of DCOIT. Gαi bound by DCOIT had an enhanced affinity for the mitochondrial calcium uniporter, consequently changing Ca2+ subcellular compartmentalization. Stimulation of Ca2+ release from the endoplasmic reticulum and blockage of Ca2+ uptake into the mitochondria resulted in a considerably higher cytoplasmic Ca2+ concentration, which then activated the phosphorylation of MEK and ERK to dysregulate hormone synthesis. Overall, by comprehensively integrating in vivo, ex vivo, in silico, and in vitro evidence, this study proposes a new mode of endocrine disrupting toxicity based on isothiazolinones, which is expected to aid the risk assessment of the chemical library and favor the mechanism-driven design of safer alternatives.

Coupling harmful algae derived nitrogen and sulfur co-doped carbon nanosheets with CeO2 to enhance the photocatalytic degradation of isothiazolinone biocide.

Removing the algae from water bodies is an effective treatment toward the worldwide frequently occurred harmful algae blooms (HAB), but processing the salvaged algae waste without secondary pollution places another burden on the economy and environment. Herein, a green hydrothermal process without any chemical addition was developed to resource the HAB algae (Microcystis sp.) into autogenous nitrogen and sulfur co-doped carbon nanosheet materials C-CNS and W-CNS, whose alga precursors were collected from pure culture and a wild bloom pond, respectively. After coupling with CeO2, the obtained optimal C-CNS/CeO2 and W-CNS/CeO2 composites photocatalytically degraded 95.4% and 88.2% of the marine pollutant 4,5-Dichloro-2-n-octyl-4-isothiazolin-3-one (DCOIT) in 90 min, significantly higher than that of pure CeO2 (63.15%). DCOIT degradation on CNS/CeO2 was further conducted under different conditions, including pH value, coexisting cations and anions, and artificial seawater. Although different influences were observed, the removal efficiencies were all above 76%. Along with the ascertained good stability and reusability in five consecutive runs, the great potential of CNS/CeO2 for practical application was validated. UV-vis DRS showed the increased light absorption of CNS/CeO2 in comparison to pure CeO2. PL spectra and photoelectrochemical measurements suggested the lowered charge transfer resistance and thereby inhibited charge recombination of CNS/CeO2. Meanwhile, trapping experiments and electron paramagnetic resonance (EPR) detection verified the primary roles of hydroxyl radical (OH) and superoxide radical (O2-) in DCOIT degradation, as well as their notably augmented generation by CNS. Consequently, a mechanism of CNS enhanced photocatalytic degradation of DCOIT was proposed. The intermediates involved in the reaction were identified by LC-QTOF-MS, giving rise to a deduced degradation pathway for DCOIT. This study offers a new approach for resourceful utilization of the notorious HAB algae waste. Besides that, photocatalytic degradation has been explored as an effective measure to remove DCOIT from the ocean.

Significant Variability in the Developmental Toxicity of Representative Perfluoroalkyl Acids as a Function of Chemical Speciation.

Current toxicological data of perfluoroalkyl acids (PFAAs) are disparate under similar exposure scenarios. To find the cause of the conflicting data, this study examined the influence of chemical speciation on the toxicity of representative PFAAs, including perfluorooctanoic acid (PFOA), perfluorobutane carboxylic acid (PFBA), and perfluorobutanesulfonic acid (PFBS). Zebrafish embryos were acutely exposed to PFAA, PFAA salt, and a pH-negative control, after which the developmental impairment and mechanisms were explored. The results showed that PFAAs were generally more toxic than the corresponding pH control, indicating that the embryonic toxicity of PFAAs was mainly caused by the pollutants themselves. In contrast to the high toxicity of PFAAs, PFAA salts only exhibited mild hazards to zebrafish embryos. Fingerprinting the changes along the thyroidal axis demonstrated distinct modes of endocrine disruption for PFAAs and PFAA salts. Furthermore, biolayer interferometry monitoring found that PFOA and PFBS acids bound more strongly with albumin proteins than did their salts. Accordingly, the acid of PFAAs accumulated significantly higher concentrations than their salt counterparts. The present findings highlight the importance of chemical forms to the outcome of developmental toxicity, calling for the discriminative risk assessment and management of PFAAs and salts.

Variability in fecal metabolome depending on age, PFBS pollutant, and fecal transplantation in zebrafish: A non-invasive diagnosis of health.

To protect the wellbeing of research animals, certain non-invasive measures are in increasing need to facilitate an early diagnosis of health and toxicity. In this study, feces specimen was collected from adult zebrafish to profile the metabolome fingerprint. Variability in fecal metabolite composition was also distinguished as a result of aging, perfluorobutanesulfonate (PFBS) toxicant, and fecal transplantation. The results showed that zebrafish feces was very rich in a diversity of metabolites that belonged to several major classes, including lipid, amino acid, carbohydrate, vitamin, steroid hormone, and neurotransmitter. Fecal metabolites had functional implications to multiple physiological activities, which were characterized by the enrichment of digestion, absorption, endocrine, and neurotransmission processes. The high richness and functional involvement of fecal metabolites pinpointed feces as an abundant source of diagnostic markers. By comparison between young and aged zebrafish, fundamental modifications of fecal metabolomes were caused by aging progression, centering on the neuroactive ligand-receptor interaction pathway. Exposure of aged zebrafish to PFBS pollutant also significantly disrupted the metabolomic structure in feces. Of special concern were the changes in fecal hormone intermediates after PFBS exposure, which was concordant with the in vivo endocrine disrupting effects of PFBS. Furthermore, it was intriguing that transplantation of young zebrafish feces efficiently mitigated the metabolic perturbation of PFBS in aged recipients, highlighting the health benefits of therapeutic strategies based on gut microbiota manipulation. In summary, the present study provides preliminary clues to evidence the non-invasive advantage of fecal metabolomics in the early diagnosis and prediction of physiology and toxicology.

Exposure to methylparaben at environmentally realistic concentrations significantly impairs neuronal health in adult zebrafish.

Methylparaben (MeP) is an emerging aquatic pollutant that is found to impact neural functions. However, it still lacks a comprehensive understanding about its neurotoxicology. The present study exposed adult zebrafish to environmentally realistic concentrations (0, 1, 3, and 10 µg/L) of MeP for 28 days, with objectives to elucidate the neurotoxic effects and mechanisms. Proteomic profiling found that MeP pollutant induced distinct mechanism of neurotoxicity as a function of sex. MeP pollutant appeared to preferentially target the neurotransmission cascade via synapse junctions. In male brain, glutamatergic neural signaling was enhanced by 10 µg/L of MeP in characteristics of higher glutamate neurotransmitter content (by 61.9%) and up-regulated glutamate receptor expression by 2.6-fold relative to the control. In MeP-exposed female brain, biomarker proteins of synapse formation and regeneration had significantly lower abundance, accounting for the blockage of synaptic neurotransmission. Furthermore, under the stress of MeP pollutant, both male and female zebrafish initiated a negative feedback mechanism along stress neuroendocrine axis by down-regulating the transcriptions of corticotropin-releasing hormone and its binding protein, which subsequently decreased blood cortisol concentrations. MeP subchronic exposure also disturbed innate immune function. In particular, significant increases in lipopolysaccharide (LPS) content by 15.6% were caused by MeP exposure in male brain, thereby inducing the synthesis of pro-inflammatory cytokines. In contrast, female brain was able to adaptively up-regulate the protein expression of blood brain barrier to inhibit the infiltration of LPS endotoxin into brain. Overall, the present findings pinpoint the potent neurotoxicity of MeP pollutant even at environmentally realistic concentrations.

Metabolomic profiles in zebrafish larvae following probiotic and perfluorobutanesulfonate coexposure.

Probiotic supplements are able to attenuate the developmental toxicity of perfluorobutanesulfonate (PFBS) pollutant. However, the underlying mechanisms remain unexplored. To this end, the present study acutely exposed zebrafish larvae for 4 days to 0 and 10 mg/L of PFBS, with or without the addition of probiotic Lactobacillus rhamnosus in the rearing water. The metabolomics approach was used to reveal the combined effects of PFBS and probiotics on metabolic dynamics, based on which gene transcriptions, enzymatic activities, and behavioral endpoints were further examined. The results showed that probiotic supplements were the major driver of the metabolomic fingerprints in coexposed zebrafish larvae. The addition of probiotic bacteria significantly decreased the methylation potential whilst up-regulating the demethylation process of genomic DNA, which may globally stimulate the gene expression to improve somatic growth. Acute exposure to PFBS significantly increased the cortisol concentration in zebrafish larvae, subsequently inducing stress response and hyperactive behavior. In contrast, probiotic supplementation promoted the degradation of cortisol, thus alleviating the stressful state. Antagonistic action of probiotics against PFBS developmental toxicity was also noted regarding the locomotor behavior. In addition, gut microbiota-mediated production of secondary bile acids was remarkably enhanced by probiotic supplements regardless of PFBS exposure. Overall, the present study underlines the efficacy of probiotic bacteria to protect zebrafish larvae from the metabolic disturbances of PFBS, thereby providing more evidence to support the application of probiotics in aquaculture and fishery as an environmentally-friendly choice.

Enhanced photocatalytic degradation of paraben preservative over designed g-C3N4/BiVO4 S-scheme system and toxicity assessment.

Paraben preservatives have been listed as emerging pollutants due to their ubiquity in various environmental matrices, especially the water bodies. How to efficiently and practically eliminate these paraben pollutants is therefore of great importance. Herein, a designed S-scheme heterojunction photocatalyst, consisting of graphitic carbon nitride (g-C3N4) and monoclinic bismuth vanadate (BiVO4), was fabricated by a facile hydrothermal synthesis and employed to treat benzyl-paraben (BzP). TEM and XPS analysis testified the intimate interaction between g-C3N4 and BiVO4, and the consequently smoothed interfacial charge transfer rendered the feasible recombination of the photoexcited electrons (from BiVO4) and holes (from g-C3N4). The as-established S-scheme system enabled the left g-C3N4 electrons and BiVO4 holes to maintain the high redox abilities and accelerated the charge separation concurrently. In particular, the g-C3N4/BiVO4 composite generated much higher photocurrent response as compared with pure g-C3N4 and BiVO4, highlighting the improved separation of photoinduced charges. Therefore, under visible light and natural solar light irradiation, the g-C3N4/BiVO4 composite showed the significantly enhanced photocatalytic degradation of BzP, which was further optimized with 5 wt% g-C3N4 in the composite. According to the Mott-Schottky plots and identified active species, the mechanism of the g-C3N4/BiVO4 S-scheme heterojunction system was illustrated. In addition, during the photocatalytic degradation process, the acute toxicity of the reaction solutions on zebrafish embryos was notably reduced. In conclusion, the demonstrated strategy to enhance the photocatalytic performance by designing S-scheme heterostructure may provide more insights into the development of high-efficiency photocatalyst towards the solar energy utilization and environmental treatment. Furthermore, photocatalytic degradation had been proved to be an efficient method for eliminating the ecological risk of paraben pollutants, warranting more attention in future work.

Insight into the formation of iodinated trihalomethanes during chlorination, monochloramination, and dichloramination of iodide-containing water.

In this study, the formation of iodinated trihalomethanes (I-THMs) was systematically evaluated and compared for three treatment processes - (i) chlorination, (ii) monochloramine, and (iii) dichloramination - under different pH conditions. The results demonstrated that I-THM formation decreased in the order of monochloramination > dichloramination > chlorination in acidic and neutral pH. However, the generation of I-THMs increased in the dichloramination < chlorination < monochloramination order in alkaline condition. Specifically, the formation of I-THMs increased as pH increased from 5 to 9 during chlorination and monochloramination processes, while the maximum I-THM formation occurred at pH 7 during dichloramination. The discrepancy could be mainly related to the stability of the three chlor (am) ine disinfectants at different pH conditions. Moreover, in order to gain a thorough insight into the mechanisms of I-THM formation during dichloramination, further investigation was conducted on the influencing factors of DOC concentration and Br-/I- molar ratio. I-THM formation exhibited an increasing and then decreasing trend as the concentration of DOC increased from 1 to 7 mg-C/L, while the yield of I-THMs increased with increasing Br-/I- molar ratio from 5:0 to 5:10. During the three processes mentioned above, similar I-THM formation results were also obtained in real water, which indicates that the excessive generation of I-THMs should be paid special attention during the disinfection of iodide-containing water.

Micropollutant removal and disinfection byproduct control by sequential peroxymonosulfate-UV treatment in water: A case study with sulfamethoxazole.

UV/peroxymonosulfate (UV/PMS) advanced oxidation process has attracted significant attention for removal of micropollutants in water. However, during practical water treatment applications, the PMS treatment must be performed before the UV treatment to achieve full contact. In this study, sulfamethoxazole (SMX) was selected as the target micropollutant. Four different operational approaches, including UV alone, PMS alone, simultaneous UV/PMS and sequential PMS-UV, were compared for their differences in SMX removal and disinfection by-product (DBP) formation potentials during chlorine-driven disinfection. Among the four approaches, UV/PMS and PMS-UV achieved over 90% removal efficiencies for SMX without substantial differences. For raw water, the trichloronitromethane (TCNM) formation potential after treatment with PMS-UV was lower than that after UV/PMS treatment. The time interval over which the PMS-UV process was conducted had little effect on the final removal efficiency for SMX. However, a brief (5 min) pre-PMS treatment significantly reduced the TCNM formation potential and the genotoxicity from DBPs. The formation risk for TCNM during chlorination increased markedly with increasing PMS dosages, and the appropriate dosage under these experimental conditions was suggested to be 0.5-1.0 mmol/L. Under alkaline conditions, PMS-UV treatment can enhance SMX degradation as well as dramatically reduced the formation potentials for haloketones, haloacetonitriles and halonitromethanes. This study suggests that proper optimization of UV/PMS processes can remove SMX and reduce its DBP formation.

Disturbances in Microbial and Metabolic Communication across the Gut-Liver Axis Induced by a Dioxin-like Pollutant: An Integrated Metagenomics and Metabolomics Analysis.

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.

Shift in skin microbiota and immune functions of zebrafish after combined exposure to perfluorobutanesulfonate and probiotic Lactobacillus rhamnosus.

Dysbiosis of fish skin microbiome and immunity by environmental pollutants are rarely studied in toxicological research in spite of their importance for fish health. In the present study, adult zebrafish were exposed to 0 and 10 µg/L of perfluorobutanesulfonate (PFBS) for 40 days, with or without the supplementation of probiotic Lactobacillus rhamnosus, with objectives to explore the interaction between PFBS pollutant and probiotic bacteria on skin mucosal microbiota and immune response. Amplicon sequencing analysis found that PFBS alone significantly disturbed the microbial community composition and abundance on the skin, favoring the growth of stress-tolerant bacteria (e.g., Deinococcus and Enhydrobacter genera). However, the administration of probiotic inhibited the dysbiosis of PFBS and shaped the skin microbiome in the combined exposure group. PFBS single exposure also promoted the production of mucus on the skin of male zebrafish, which may be related to the growth of Limnobacter bacteria. In contrast, probiotic supplements remarkably improved the immune functions in male skin mucus from the combined group, as evidenced by the consistent increases in lysozyme activity, immunoglobulin concentrations and peroxidase activity. Overall, the present study provides the first clue about the singular and combined effects of PFBS and probiotic on skin microbiota and immunity, highlighting the beneficial action of probiotic L. rhamnosus against PFBS stress.

Interaction between probiotic additive and perfluorobutanesulfonate pollutant on offspring growth and health after parental exposure using zebrafish.

Perfluorobutanesulfonate (PFBS) pollutant and probiotic bacteria can interact to affect the reproductive outcomes of zebrafish. However, it is still unexplored how the growth and health of offspring are modulated by the combination of PFBS and probiotic. In the present study, adult zebrafish were exposed to 0 and 10 µg/L PFBS for 40 days, with or without dietary supplementation of probiotic Lactobacillus rhamnosus. After parental exposure, the development, growth and viability of offspring larvae were examined, with the integration of molecular clues across proteome fingerprint, growth hormone/insulin-like growth factor (GH/IGF) axis, calcium homeostasis, hypothalamic-pituitary-adrenal (HPA) axis and nutrient metabolism. Parental probiotic supplementation significantly increased the body weight and body length of offspring larvae. Despite the spiking of PFBS, larvae from the combined exposure group still had longer body length. RNA processing and ribosomal assembly pathways may underlie the enhancement of offspring growth by probiotic bacteria. However, the presence of PFBS remarkably increased the concentrations of cortisol hormone in offspring larvae as means to cope with the xenobiotic stress, which required more energy production. As evidenced by the proteomic analysis, the addition of probiotic bacteria likely alleviated the energy metabolism disorders of PFBS, thus allocating more energy for the larval offspring growth from the combined group. It was noteworthy that multiple molecular disturbances caused by PFBS were antagonized by probiotic additive. Overall, the present study elucidated the intergenerational interaction between PFBS and probiotic on offspring growth and health after parental exposure.

Fingerprinting fecal DNA and mRNA as a non-invasive strategy to assess the impact of polychlorinated biphenyl 126 exposure on zebrafish.

In toxicological studies, experimental animals are generally subjected to dissection to obtain the tissues of concern, which causes great harm to the animals. In this regard, it is necessary to test and develop a non-invasive strategy to prevent the animals from anthropic injury when achieving scientific objectives. Therefore, zebrafish fecal DNA and mRNA pools were assessed by using metagenomic and transcriptomic analyses based on their potential to diagnose toxicological impairment of polychlorinated biphenyl (PCB) 126, a model persistent organic pollutant. The results showed that there was abundant zebrafish DNA and mRNA in the feces, which were, however, associated with contrasting profiles of physiological activities. As compared to DNA fragments, fecal mRNA provided a better representation of zebrafish physiological status. PCB126 exposure dramatically shifted the composition of fecal zebrafish DNA and mRNA as a function of sex. The differential mRNA caused by PCB126 clearly identified the toxicological fingerprint of PCB126. In summary, this study provides preliminary clues about the potential of fecal genes (mRNA in particular) in the development of non-invasive toxicological approaches. In the future, it is expected that more works will be conducted to screen sensitive diagnostic biomarkers from feces to increase the rate and reduce the cost of ecological risk assessment.

Unexpected Observations: Probiotic Administration Greatly Aggravates the Reproductive Toxicity of Perfluorobutanesulfonate in Zebrafish.

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.

Probiotic Modulation of Lipid Metabolism Disorders Caused by Perfluorobutanesulfonate Pollution in Zebrafish.

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 < 0.001; r > 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 ß-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.

Perfluorobutanesulfonate Exposure Skews Sex Ratio in Fish and Transgenerationally Impairs Reproduction.

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.

Parental Exposure to Perfluorobutanesulfonate Impairs Offspring Development through Inheritance of Paternal Methylome.

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.

Acute exposure to triphenyl phosphate (TPhP) disturbs ocular development and muscular organization in zebrafish larvae.

Triphenyl phosphate (TPhP) is an organophosphate flame retardant that is frequently detected in the environments. TPhP exposure is known to cause developmental toxicity. However, the underlying molecular mechanisms remain underestimated. In the present study, zebrafish embryos were acutely exposed to 0, 4 and 100 µg/L TPhP until 144 h post-fertilization. Profiles of differentially expressed proteins were constructed using a shotgun proteomic. With the input of differential proteins, principal component analysis suggested different protein expression profiles for 4 and 100 µg/L TPhP. Gene ontology and KEGG pathway analyses further found that effects of TPhP at 4 µg/L targeted phagosome and lysosome activity, while 100 µg/L TPhP mainly affected carbohydrate metabolism, muscular contraction and phagosome. Based on proteomic data, diverse bioassays were employed to ascertain the effects of TPhP on specific proteins and pathways. At gene and protein levels, expressions of critical visual proteins were significantly changed by TPhP exposure, including retinoschisin 1a, opsins and crystallins, implying the impairment of ocular development and function. TPhP exposure at 100 µg/L also altered the abundances of diverse muscular proteins and disordered the assembly of muscle fibers. Effects of TPhP on visual development and motor activity may be combined to disturb larval swimming behavior. In summary, current results provided mechanistic clues to the developmental toxicities of TPhP. Future works are inspired to broaden the toxicological knowledge of TPhP based on current proteomic results.

Organic ultraviolet (UV) filters in the South China sea coastal region: Environmental occurrence, toxicological effects and risk assessment.

Organic ultraviolet (UV) filters are common ingredients of personal care products and occur ubiquitously in the aquatic environment; however, little is known about their distribution in and potential effects to the marine environment. This study reports the occurrence, toxicological effects and risk assessment of eleven commonly consumed UV filters in marine surface water collected from the South China Sea (SCS) coastal region. The concentrations of UV filters ranged from

Multigenerational Disruption of the Thyroid Endocrine System in Marine Medaka after a Life-Cycle Exposure to Perfluorobutanesulfonate.

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.