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This study purposes to assess the cytotoxicity of 1-dodecyl-3-methylimidazolium chloride ([C 12 min]Cl) in human hepatocellular carcinoma (HepG2) cells. To this end, HepG2 cells were exposed to a range concentration of [C 12 min]Cl and evaluated cell viability, genotoxicity, oxidative stress, apoptosis, cell cycle, and apoptosis-related gene expression to determine cytotoxicity. The outcomes showed that [C 12 min]Cl curbed HepG2 cell growth and reduced cell viability in a concentration- and time-dependent manner. Moreover, our assay results also revealed that exposure to [C 12 min]Cl prompted DNA damage and apoptosis, reduced SOD and GSH content, enhanced MDA level, and changed the cell cycle of HepG2 cells. In addition, [C 12 min] Cl caused alters in the expression levels of p53, Bax, and Bcl-2, indicating that p53 and Bcl-2 family may be involved in the cytotoxicity and apoptosis of HepG2 cells induced by [C 12 min]C1. In summary, these results indicate that [C 12 min]Cl exerts genotoxicity, physiological toxicity and prompts apoptosis in HepG2 cells, and is not an alleged green solvent., (© 2020 Wiley Periodicals, Inc.)

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]

This study was a preliminary step to evaluate the acute toxicity of 1-methyl-3-octylimidazolium chloride ([C8mim]Cl) on loach (Misgurnus anguillicaudatus) by determining the effects on hepatic antioxidant enzyme activities and by the comet assay. The results showed that [C8mim]Cl had acute toxicity at concentrations above 20 mg L−1, inducing oxidative stress and genotoxicity on fish liver cells. In respect to enzyme activities, [C8mim]Cl induced changes in the activities of superoxide dismutase, catalase, and glutathione content the livers of fish exposed at 20–80 mg L−1. [C8mim]Cl at the same exposure level caused a remarkable increase in malondialdehyde level. The comet assay indicated that [C8mim]Cl at 20–80 mg L−1induced genotoxicity in liver cells. With increased exposure concentration and time, the two comet parameters trailing rate and tail moment were significantly increased, with significant differences (P< 0.05) observed between control group and each treatment group. The present study shows that ionic liquids can be a threat to the health of aquatic organism when accidentally released to aquatic ecosystems. [ABSTRACT FROM PUBLISHER]

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]

Abstract Ionic liquids have garnered increasing attention due to their capacity for low vapor pressure, lack of flammability, designability, good stability, and as a asubstitute for conventional organic solvents. However, their toxicity to various organisms has caused growing concern in recent years. Our study aims to evaluate the toxicity of 1-hexadecyl-3-methylimidazolium chloride ([C 16 min]Cl) to human hepatocellular carcinoma (HepG2) cells, including cell viability, genotoxicity, oxidative stress, apoptosis, cell cycle, and apoptosis-related gene expression. Our results with HepG2 cells suggested that [C 16 min]Cl inhibited cellular growth, decreased cell viability, induced DNA damage and apoptosis, inhibited superoxide dismutase, decreased glutathione content, increased cellular malondialdehyde levels as well as altering the cell cycle. Moreover, the induction of [C 16 min]Cl altered the transcription of p53 , Bax and Bcl-2 , which are critical for controlling cell cycles progression and death, which suggests its involvement with cytotoxicity and apoptosis induced by [C 16 min]Cl in HepG2 cells. Taken together, these results revealed that [C 16 min]Cl exerted genotoxicity, oxidative stress and induced apoptosis in HepG2 cells; hence, it is not a healthy solvent. Highlights • [C 16 min]Cl is cytotoxic to HepG2 cells. • [C 16 min]Cl inhibits HepG2 cells growth and decreases their viabilities. • [C 16 min]Cl exerts genotoxicity, oxidative stress and induces apoptosis in HepG2 cells. [ABSTRACT FROM AUTHOR]

The occurrence and accumulation of microplastics in wildlife and humans have become a serious global scale concern over the last decade. To evaluate the potential toxic effects of PVC (polyvinyl chloride) microplastics in freshwater fish larvae, we conducted chronic 30-day and 60-day dietary exposure using Cyprinus carpio var. larvae. We exposed the larvae to four treatments with different microplastic concentrations (10%, 20%, and 30%) using food rationed diets, in conjunction with a non-plastic control. The results indicated that microplastics significantly inhibited weight gain and growth under all PVC treatments, compared to the control group. SOD (superoxide dismutase) and CAT (catalase) activities were analyzed, and an inverse relationship between them was observed. The activities of GPx (glutathione peroxidase) initially ascended and then descended with increased PVC concentrations following 30 days of exposure. A dose dependent downtrend was observed after 60 days of exposure. Malondialdehyde (MDA) levels were significantly reduced upon exposure to different concentrations of microplastics in various tissues. Altered antioxidant-related gene expression was observed in the livers of larvae exposed to the PVC microplastics. The transcription of CYP1A and GSTa initially increased, and then decreased under higher microplastics concentrations following 30 days of exposure. Furthermore, histological studies revealed cytoplasmic vacuolation in the liver under exposure to 20% and 30% microplastics. This investigation provided basic toxicological data toward elucidating and quantifying the impacts of PVC microplastics on freshwater organisms. Unlabelled Image • PVC microplastics inhibited weight gain and body length growth of carp larvae. • Antioxidant activities were altered following PVC microplastics exposure. • PVC microplastics influenced the expression levels of CYP1A , GSTpi , and GSTa. • Histological changes occurred in the livers of fish exposed to PVC microplastics. [ABSTRACT FROM AUTHOR]