Emodin is an anthraquinone secondary metabolite produced by several species of plants and fungi. Emodin is known for its pharmacological versatility, and, in the textile industry, for its good dyeing ...properties. However, its use in the textile industry can result in the formation and disposal of large volumes of wastewater. Emodin mutagenicity has been shown in bacteria and in human cells, but little is known about its possible toxic, genotoxic, or mutagenic effects in aquatic organisms. We have evaluated the eco/genotoxicity of emodin to aquatic organisms. Emodin was toxic to Daphnia similis (EC50 = 130 μg L−1) and zebrafish embryos (LC50 = 25 μg L−1). No toxicity was observed for Raphidocelis subcapitata, Ceriodaphnia dubia, or Parhyale hawaiensis. Additional biochemistry/molecular studies are needed to elucidate the toxic/mutagenic pathways of emodin in aquatic organisms. The PNEC value for emodin was 0.025 μg L−1. In addition to mutagenicity in the Salmonella/microsome assay, emodin was mutagenic in the micronucleus assay in the amphipod P. hawaiensis. Among the anthraquinone dyes tested to date, natural or synthetic, emodin was the most toxic to aquatic species.
•Emodin is toxic to Daphnia similis and Danio rerio embryos.•Among the organisms studied, Danio rerio embryo was the most sensitive to emodin.•Emodin is mutagenic to Parhyale hawaiensis.•Emodin is more toxic than dermorubin and dermocybin to aquatic species.
Furan is a widespread endogenous contaminant in heat-processed foods that can accumulate rapidly in the food chain and has been widely detected in foods, such as wheat, bread, coffee, canned meat ...products, and baby food. Dietary exposure to this chemical may bring health risk. Furan is classified as a possible category 2B human carcinogen by the International Agency for Research on Cancer, with the liver as its primary target organ. Hepatic fibrosis is the most important nontumoral harmful effect of furan and also an important event in the carcinogenesis of furan. Although the specific mechanism of furan-induced liver fibrosis is still unclear, it may involve oxidative stress and genetic toxicity, in which the activation of cytochrome P450 2E1 (CYP2E1) may be the key event. Thus, we conducted a study using an integrating multi-endpoint genotoxicity platform in 120-day in vivo subchronic toxicity test in rats. Results showed that the rats with activated CYP2E1 exhibited DNA double-strand breaks in D4, gene mutations in D60, and increased expression of reactive oxygen species and nuclear factor erythroid 2-related factor 2 in D120. Necrosis, apoptosis, hepatic stellate cell activation, and fibrosis also occurred in the liver, suggesting that furan can independently affect liver fibrosis through oxidative stress and genotoxicity pathways. Point of Departure (PoD) was obtained by benchmark-dose (BMD) method to establish health-based guidance values. The human equivalent dose of PoD derived from BMDL05 was 2.26 μg/kg bw/d. The findings laid a foundation for the safety evaluation and risk assessment of furan and provided data for the further construction and improvement of the adverse outcome pathway network in liver fibrosis.
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•An integrated genotoxicity platform was applied to explore the AOP of furan.•Furan may induce gene mutation in a cumulative way, independent of oxidative stress.•The AOP of CYP2E1 activation leading to liver fibrosis was preliminary established.•BMDLs of key events from AOP are more protective than values from apical endpoints.
Ibuprofen (IBP) is an anti-inflammatory drug found in aquatic environments, potentially toxic for the biota. We exposed the test fish C. decemmaculatus to two environmentally relevant concentrations ...(50 and 100 μg IBP/L) for 4 and 12 d and evaluated the effect on some biomarkers. Micronucleus test, nuclear abnormality test and comet assay indicated cyto-genotoxicity at both concentrations and exposure periods. Oxidative stress and biochemical biomarkers were not affected, excepting muscle AChE activity for 4 d. Muscle metabolic biomarkers showed significant decrease in ETS, lipid and protein content, while carbohydrate content was not affected. The CEA index increased at the lower IBP concentration for 4 and 12 d, possibly due to changes in body energy reserves. A full-factorial GLM performed to assess the effects of IBP and exposure times showed that the metabolic and genotoxicity biomarkers were the most sensitive to IBP toxicity, mainly at 50 μg IBP/L for 4 d.
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•Exposure of Cnesterodon decemmaculatus to IBP was more toxic at 4 than at 12 d.•Exposure of Cnesterodon decemmaculatus was more toxic at 50 than at 100 μg IBP/L.•Metabolic and genotoxicity biomarkers were more sensitive to IBP toxicity than oxidative stress biomarkers.•CEA index was affected by the interaction of IBP concentration and exposure time.•IBP concentration-exposure time interaction may compromise fish energy budget.
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•ZrO2-CaCr2O4-BiOIO3 nanocomposite were synthesised by facile co-precipitation method.•The NCs exhibits excellent photodegradation of cefixime and doxycycline.•The end product ...toxicity was evaluated against E.coli and S.epidermis.•Investigation of genotoxicity towards Allium cepa.•Elucidation of photodegradation pathway using ECOSAR software.
Today, diverse form of antibiotic drugs has been used extensively for the treatment of various microbe related diseases. The improper handling and overusage of these antibiotics have tremendously affected the aquatic system. Therefore, the development of low cost and highly efficient photocatalyst for the effective degradation of antibiotics is paramount for the remediation of toxic pollutants in water bodies. In the present study, the ternary ZrO2-CaCr2O4-BiOIO3 nanocomposite (NC) has been newly fabricated under simple chemical co-precipitation technique. The developed ternary NC was investigated for the photodegradation of cefixime (CFX) and doxycycline (DOX) under visible light irradiation. The prepared NC was characterized by various physiochemical analysis including HR-TEM, SEM, UV–vis DRS, XPS, FT-IR, ESR, PL, Raman, EIS, and N2 adsorption and desorption analysis. The reusability of the photocatalyst was tested by performing six consecutive cycles. The toxicity of the degraded end products of CFX and DOX has been evaluated against E. coli and S. epidermis. The fabricated NC was investigated for its photodegradation efficiency under different parameters such as pH, antibiotic concentration, and NC dosage. The photodegradation mechanism was elucidated using scavenging study, and ESR analysis. The TOC results confirmed the complete mineralisation of CFX and DOX. Also, the possible degradation pathway of CFX and DOX was determined based on GC–MS analysis. The fabricated NC were investigated for the genotoxicity towards Allium cepa. The present study opens up a new insight for using ZrO2-CaCr2O4-BiOIO3 photocatalyst for remediation of pharmaceutical pollutant.
Human liver-derived metabolically competent HepaRG cells have been successfully employed in both two-dimensional (2D) and 3D spheroid formats for performing the comet assay and micronucleus (MN) ...assay. In the present study, we have investigated expanding the genotoxicity endpoints evaluated in HepaRG cells by detecting mutagenesis using two error-corrected next generation sequencing (ecNGS) technologies, Duplex Sequencing (DS) and High-Fidelity (HiFi) Sequencing. Both HepaRG 2D cells and 3D spheroids were exposed for 72 h to
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-nitrosodimethylamine (NDMA), followed by an additional incubation for the fixation of induced mutations. NDMA-induced DNA damage, chromosomal damage, and mutagenesis were determined using the comet assay, MN assay, and ecNGS, respectively. The 72-h treatment with NDMA resulted in concentration-dependent increases in cytotoxicity, DNA damage, MN formation, and mutation frequency in both 2D and 3D cultures, with greater responses observed in the 3D spheroids compared to 2D cells. The mutational spectrum analysis showed that NDMA induced predominantly A:T → G:C transitions, along with a lower frequency of G:C → A:T transitions, and exhibited a different trinucleotide signature relative to the negative control. These results demonstrate that the HepaRG 2D cells and 3D spheroid models can be used for mutagenesis assessment using both DS and HiFi Sequencing, with the caveat that severe cytotoxic concentrations should be avoided when conducting DS. With further validation, the HepaRG 2D/3D system may become a powerful human-based metabolically competent platform for genotoxicity testing.
Carbon black exposure causes oxidative stress, inflammation and genotoxicity. The objective of this systematic review was to assess the contributions of primary (i.e. direct formation of DNA damage) ...and secondary genotoxicity (i.e. DNA lesions produced indirectly by inflammation) to the overall level of DNA damage by carbon black. The database is dominated by studies that have measured DNA damage by the comet assay. Cell culture studies indicate a genotoxic action of carbon black, which might be mediated by oxidative stress. Many in vivo studies originate from one laboratory that has investigated the genotoxic effects of Printex 90 in mice by intra-tracheal instillation. Meta-analysis and pooled analysis of these results demonstrate that Printex 90 exposure is associated with a slightly increased level of DNA strand breaks in bronchoalveolar lavage cells and lung tissue. Other types of genotoxic damage have not been investigated as thoroughly as DNA strand breaks, although there is evidence to suggest that carbon black exposure might increase the mutation frequency and cytogenetic endpoints. Stratification of studies according to concurrent inflammation and DNA damage does not indicate that carbon black exposure gives rise to secondary genotoxicity. Even substantial pulmonary inflammation is at best only associated with a weak genotoxic response in lung tissue. In conclusion, the review indicates that nanosized carbon black is a weak genotoxic agent and this effect is more likely to originate from a primary genotoxic mechanism of action, mediated by e.g. oxidative stress, than inflammation-driven (secondary) genotoxicity.
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