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Ibuprofen (IBU), as a commonly used non-steroidal anti-inflammatory drug (NSAID) and pharmaceutical and personal care product (PPCP), is frequently prescribed by doctors to relieve pain. It is widely released into environmental water and soil in the form of chiral enantiomers by the urination and defecation of humans or animals and by sewage discharge from wastewater treatment plants. This study focused on the alteration of metabolism in the adult zebrafish ( Danio rerio ) brain after exposure to R-(-)-/S-(+)-/rac-IBU at 5 μg L −1 for 28 days. A total of 45 potential biomarkers and related pathways, including amino acids and their derivatives, purine and its derivatives, nucleotides and other metabolites, were observed with untargeted metabolomics. To validate the metabolic disorders induced by IBU, 22 amino acids and 3 antioxidant enzymes were selected to be quantitated and determined using targeted metabolomics and enzyme assay. Stereoselective changes were observed in the 45 identified biomarkers from the untargeted metabolomics analysis. The 22 amino acids quantitated in targeted metabolomics and 3 antioxidant enzymes determined in enzyme assay also showed stereoselective changes after R-(-)-/S-(+)-/rac-IBU exposure. Results showed that even at a low concentration of R-(-)-/S-(+)-/rac-IBU, disorders in metabolism and antioxidant defense systems were still induced with stereoselectivity. Our study may enable a better understanding of the risks of chiral PPCPs in aquatic organisms in the environment. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the oxidative stress process and bioaccumulation the racemic/(−)-/(+)- 2,2ʹ,3,4ʹ,6-pentachlorobiphenyl were administered to adult zebrafish ( Danio rerio ) after prolonged exposure of 56-days uptake and 49-days depuration experiments. Stereoselective accumulation was observed in adult samples after racemic exposure as revealed by decreased enantiomer fractions. The two enantiomers of PCB91 accumulated at different rates with logBCF k values close to 3.7, suggesting that they were highly hazardous and persistent pollutants. Exposure to racemic/(−)-/(+)- PCB91 stereoselectively induced oxidative stress owing to changes in reactive oxygen species, malondialdehyde contents, antioxidant enzyme activities and gene expressions in brain and liver tissues. In addition, the stereoselective relationship between bioconcentration and oxidative stress were also presented in this study. Our findings might be helpful for elucidating the environmental risk of the two enantiomers of PCB91 that induce toxicity in aquatic organisms. [ABSTRACT FROM AUTHOR]

This paper was designed to study stereoselective enrichment and changes in gene expression when zebrafish (Danio rerio) embryo-larvae were exposed to racemic, (-)- or (+)- PCB149 (2,2’,3,4’,5’,6- hexachlorobiphenyl). Based on bioconcentration analysis, non-racemic enrichment was significantly observed after racemic exposure. No isomerization between the two isomers was found after (-)/(+)-PCB149 exposure. Furthermore, based on gene expression-data mining, CYPs genes (cyp2k6, cyp19a1b, and cyp2aa4) were differential genes after (+)-PCB149 exposure. No obvious differences of dysregulation of gene expression caused by racemic and (-)-PCB149, were observed in embryo-larvae. The above results suggested that (-)-PCB149 could be considered as the main factor causing the dysregulation of gene expression in embryo-larvae after racemic exposure; and (+)-PCB149 should be pursued apart from the racemate, when considering the toxicity of chiral PCB149. Thus, the information in our study could provide new insights to assess the environmental risk of chiral PCBs in aquatic systems. [ABSTRACT FROM AUTHOR]

Mefentrifluconazole is a new chiral triazole fungicide with high efficiency and broad spectrum. Zebrafish embryos, larvae and adults were exposed to mefentrifluconazole racemate and enantiomers to investigate aquatic toxicity of mefentrifluconazole at the enantiomer level. Acute toxicity tests were conducted to determine the lethality of mefentrifluconazole. The developmental toxicity of mefentrifluconazole to embryos and larvae was also assessed during acute exposure. Besides, the growth parameters of adults were evaluated after 14 days' exposure. The 96-h LC 50 ranges of rac-, R-(−)- and S-(+)-mefentrifluconazole to all zebrafish life-stages were 0.753–1.198, 1.092–2.022 and 0.583–1.056 mg/L respectively. Larvae were the most sensitive to mefentrifluconazole in terms of lethality, followed by embryos and adults. During acute exposure, morphological deformities caused by mefentrifluconazole, such as yolk sac edema and pericardial edema in embryos, as well as pericardial edema and spinal curvature in larvae were discovered. Besides, mefentrifluconazole induced significant developmental defects, including inhibited heartbeat and reduced body length in both embryos and larvae. After 14 days' mefentrifluconazole exposure, severe growth inhibition in adult zebrafish was observed. Mefentrifluconazole shows enantioselective toxicity in all stages of zebrafish, and the order of toxicity is S-(+)-mefentrifluconazole > rac-mefentrifluconazole > R-(−)-mefentrifluconazole. Further study is required to explore the specific enantioselective mechanism. Our findings enable a better understanding of the potential risk of mefentrifluconazole to aquatic ecosystems at the enantiomer level. [Display omitted] • Mefentrifluconazole showed strong lethality to zebrafish. • Mefentrifluconazole induced severe developmental effects on multiple stages of zebrafish. • S-(+)-mefentrifluconazole exerted higher toxicity to zebrafish than R-(−)-mefentrifluconazole. [ABSTRACT FROM AUTHOR]

Cyhalofop-butyl is a selective herbicide widely employed in paddy field, which can transfer into aquatic environments. However, details of the environmental risk and aquatic toxicity of cyhalofop-butyl have not been fully investigated. In this study, zebrafish ( Danio rerio ) embryos were exposed to a range of cyhalofop-butyl until 120 hour post-fertilization (hpf) to assess embryonic toxicity of the chemical. Our results demonstrated that cyhalofop-butyl was highly toxic to zebrafish embryos, with concentration-dependent negative effects in embryonic development. In addition, exposure to cyhalofop-butyl resulted in significant increases in reactive oxygen species (ROS) production and cell apoptosis in heart area. The mRNA levels of the genes related to oxidative stress and apoptosis were also altered significantly after cyhalofop-butyl exposure. Moreover, the activity of capspase-9 and caspase-3 were significantly increased. Therefore, we speculated that oxidative stress-induced apoptosis should be responsible for abnormal development during embryogenesis after cyhalofop-butyl exposure. [ABSTRACT FROM AUTHOR]

We report here an investigation of the mechanisms contributing to the divergent sensitivity toward the triazole fungicide difenoconazole of zebrafish ( Danio reio ) during different life stages. Adult and embryonic zebrafish were exposed to three different concentrations of difenoconazole (0.01, 0.5 and 1.0 mg/L). The death rate, bioaccumulation of difenoconazole, oxidative stress parameters and transcription of related genes were tested at 4 and 8 days post-exposure (dpe). The death rate for adult zebrafish was much higher than that of the embryos at an exposure concentration of 1.0 mg/L at both 4 and 8 dpe. The concentrations of difenoconazole in both the embryos and adult fish were similar, except for the group exposed to 0.01 mg/L difenoconazole. A decrease in antioxidant enzyme activities was observed in both the embryos and the livers of adult fish after exposure to difenoconazole. Significant lipid peroxidation was found in the livers of adult fish in all exposure groups at 8 dpe, but was not observed in the treated embryos. The gene transcription response of the embryos toward difenoconazole was different from that in the livers of adult fish at 4 dpe. At 8 dpe, the modification in the transcription of the tested genes in the embryos and adult fish was similar, except for the genes related to the synthesis of sterols. [ABSTRACT FROM AUTHOR]

Fluoxetine is frequently detected in aquatic environment, and chronic FLX exposure exhibits adverse effects on aquatic communities. Its chirality makes the adverse effects more complicated. This study aimed at the enantioselective cardiotoxicity in developmental zebrafish induced by racemic (rac-)/S-/R-fluoxetine. The accumulation profiles demonstrated that biotransformation of fluoxetine to norfluoxetine occurred during rac-fluoxetine exposure, with a higher enrichment of S-norfluoxetine than R-norfluoxetine. Heart malformations including pericardial edema, circulation abnormalities, and thrombosis were observed, and enantioselective changes also occurred. According to H&E staining and Masson's trichrome staining, the loose severity of cardiac structure and cardiac fibrosis in rac-norfluoxetine treated group was worse than that in fluoxetine treated groups. Results of toxicity-associated parameters in our homochiral enantiomers' exposure also indicated that the toxicity induced by S-fluoxetine was more severe than R-fluoxetine. Enantioselective arrhythmia in developmental zebrafish after chiral fluoxetine exposure could be caused by myocardial fibrosis, abnormal developmental processes, and the biotransformation of fluoxetine to norfluoxetine could make that worse. Our findings can be used to assess the environmental risk of the two enantiomers of fluoxetine that induce cardiotoxicity in aquatic organisms. Image 1 • Chiral fluoxetine exposure induced enantioselective arrhythmia in developmental zebrafish. • Biotransformation of fluoxetine to norfluoxetine could make arrhythmia worse. • Higher enrichment of S-norfluoxetine was observed during rac-fluoxetine exposure. • Cardiotoxicity induced by S-fluoxetine were more severe than R-fluoxetine. [ABSTRACT FROM AUTHOR]

Thifluzamide is a fungicide widely used to control crop diseases, and it therefore constitutes a hazard to the environment. In this study, zebrafish were selected to assess the aquatic toxicity of thifluzamide. The acute and development toxicity of thifluzamide to embryos, larvae, and adult zebrafish were measured and the corresponding 96 h-LC 50 values were as follows: adult fish (4.19 mg/L)