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The levels of the chlorinated organic compound Dechlorane Plus (DP) are increasing in aquatic ecosystems. To investigate the adverse effects of DP on aquatic animals, common carp (Cyprinus carpio) were subjected to three different DP concentrations (30 μg L−1, 60 μg L−1, and 120 μg L−1) for 1 d, 15 d, and 30 d. Histology and the hepatic and cerebral expression levels of several key antioxidant, detoxification, and apoptotic factors were then examined. Histopathological inspections showed that the liver and brain were severely damaged in carp exposed to 60 μg L−1 and 120 μg L−1 DP. Relative to the controls, the superoxide dismutase and glutathione activity levels and the malondialdehyde content were also changed in livers and brains exposed to DP. Besides, significant alterations in the expression levels of the inflammatory cytokines IL-1β, IL-6, and IL-10 were observed in the livers of carp subjected to DP. Relative to the control, the brains of DP-exposed carp presented with significantly upregulated IL-1β and IL-6 in carp treated with 120 μg L−1 DP for 30 d. The transcription levels of hepatic cyp2b4, cyp1b1, and cyp3a138 were all increased compared with the untreated at all DP exposure concentrations. The aforementioned results suggest that DP exposure perturbs fish metabolism and causes liver injury by inhibiting antioxidant enzyme activity, increasing lipid peroxidation, promoting inflammation, and inducing cell apoptosis. This information and the analytical methodology used to acquire it may form the basis for future ecological risk assessments on DP and related xenobiotics in aquatic animals. [ABSTRACT FROM AUTHOR]

Microplastics have become a worldwide pollutant, widely discovered in soil, air and aquatic environment. Microplastics have been found in habitats where crayfish (Procambarus clarkii) cultivated, but the impact of microplastics on crayfish remains unclear. In this study, after 21-day dietary exposure, polyethylene (PE) particles were found to accumulate in intestine, hepatopancreas, gills and hemolymph of crayfish. Furthermore, PE particles can still be detected in these tissues after a 7-day depuration in clean water. PE retained in these tissues caused oxidative stress responses, as indicated by the change of oxidative-stress-related index, such as the increase of H 2 O 2 level and SOD activity. PE exposure also caused hemocytic encapsulation in crayfish hepatopancreas and increase of mucus secretion in intestine. Moreover, PE exposure affected the microbiota balance in crayfish, by reducing the total microbiota abundance and altering the proportions of many bacterial families. Interestingly, results showed that PE exposure led to of lower numbers of hemocytes and declination of phenoloxidase activity. Finally, PE exposure induced the expression of immune-related genes, including transcription factors and antimicrobial peptides. Taken these together, we conclude that PE microplastics exert considerable toxic effects on crayfish and are a potential threat to crayfish aquaculture and consumption. This study provides basic toxicological data toward quantifying and illuminating the impact of PE microplastics on freshwater animals. [Display omitted] • Polystyrene microplastics accumulated in several tissues of crayfish and caused histopathological changes. • Polystyrene microplastics induced oxidative stress and immune responses in crayfish. • Polystyrene microplastics induced gut microbiota dysbiosis in crayfish. [ABSTRACT FROM AUTHOR]

Nanomaterials have attracted much attention in the biomedical field. Black phosphorus quantum dots (BPQDs) have shown great potential in biomedical applications, but their potential risks to biosafety and environmental stability have not been fully evaluated. In the present study, zebrafish (Danio rerio) embryos were exposed to 0, 2.5, 5 and 10 mg/L BPQDs from 2 to 144 h post-fertilization (hpf) to explore developmental toxicity. The results showed that exposure to BPQDs for 96 h induced developmental malformations (tail deformation, yolk sac edema, pericardial edema, and spinal curvature) in zebrafish embryos. ROS and antioxidant enzyme activities (CAT, SOD, MDA and T-AOC) were substantially altered and the acetylcholinesterase (AChE) enzyme activity was significantly decreased in the BPQDs exposed groups. Locomotor behavior was inhibited after BPQDs exposure for 144 h in zebrafish larvae. A significant increase in 8-OHdG content indicates DNA oxidative damage in embryos. In addition, obvious apoptotic fluorescence signals were detected in the brain, spine, yolk sac and heart. At the molecular level, the mRNA transcript levels of key genes related to skeletal development (igf1, gh, MyoD and LOX), neurodevelopment (gfap, pomca, bdnf and Mbpa), cardiovascular development (Myh6, Nkx2.5, Myl7, Tbx2b, Tbx5 and Gata4) and apoptosis (p53, Bax, Bcl-2, apaf1, caspase-3 and caspase-9) were abnormal after BPQDs exposure. In conclusion, BPQDs induced morphological malformations, oxidative stress, locomotor behavior disorders, DNA oxidative damage and apoptosis in zebrafish embryos. This study provides a basis for further study on the toxic effects of BPQDs. [Display omitted] • BPQDs caused developmental toxicity in the zebrafish embryos. • BPQDs induced oxidative stress, oxidative DNA damage and apoptosis in zebrafish embryos. • BPQDs induced developmental neurotoxicity and decreased locomotor behavior. [ABSTRACT FROM AUTHOR]