F-53B induces hepatotoxic effects and slows self-healing in ulcerative colitis in mice.

Chlorinated polyfluorinated ether sulfonate (F-53 B) is a distinct substitute for perfluorooctane sulphonate. It has been reported to be biologically toxic to mammals, causing enteric toxicity, liver toxicity and neurotoxicity. However, studies about the effects of F-53 B on patients with gastrointestinal diseases such as inflammatory bowel disease are very limited. In this study, whether the toxic impacts of F-53 B on the gut and liver can be exacerbated in mice with colitis was explored. The sensitivity of mice with acute colitis caused by dextran sulfate sodium salt (DSS) to F-53 B was compared with that of healthy mice. The mice were administered water containing F-53 B at doses of 10 and 100 µg/L sequentially for two weeks, respectively. F-53 B exposure exacerbated DSS-induced colonic inflammation, including inducing shortening of colon length, inflammatory cell infiltration and more severe histopathological symptoms. In addition, F-53 B administration significantly increased the levels of inflammatory cytokines, including interleukin (IL)-1, IL-6 and tumour necrosis factor-α, in the plasma of mice with enteritis compared with control group. F-53 B impaired intestinal integrity of mice with colitis by downregulating Claudin-1 and antimicrobial peptide-related genes while elevating serum lipopolysaccharide levels. In addition, in mice with colitis, F-53 B increased the levels of serum total cholesterol, triglyceride, low-density lipoprotein cholesterol, aspartate aminotransferase, and alanine aminotransferase, resulted in more severe liver inflammation and increased the level of genes related to the Gasdermin D-mediated pyrolysis. Conclusively, our results indicated that F-53 B delayed the self-healing of ulcerative colitis (UC) and caused liver inflammation in mice. This study provided some new insights into the health risks of F-53 B and raises concerns about the health of individuals with UC.

6:2 Cl-PFESA has the potential to cause liver damage and induce lipid metabolism disorders in female mice through the action of PPAR-γ.

6:2 Cl-PFESA is a polyfluoroalkyl ether with high environmental persistence that has been confirmed to have significant adverse effects on animals. In this study, 6-week-old female C57BL/6 mice were exposed to 0, 1, 3 and 10 µg/L 6:2 Cl-PFESA for 10 weeks to estimate the hepatotoxicity of 6:2 Cl-PFESA and explore its underlying molecular mechanism. The results indicated that 6:2 Cl-PFESA preferentially bioaccumulated in the liver and induced hepatic cytoplasmic vacuolation and hepatomegaly in mice. In addition, serum metabolic profiling showed that 6:2 Cl-PFESA exposure caused an abnormal increase in amino acids and an abnormal decrease in acyl-carnitine, which interfered with fatty acid transport and increased the risk of metabolic diseases. Further experiments showed that 6:2 Cl-PFESA formed more hydrogen bonds with PPAR-γ than PFOS, Rosi and GW9662, and the binding affinity of 6:2 Cl-PFESA toward PPAR-γ was the highest among the ligands. 6:2 Cl-PFESA promoted the differentiation of 3T3-L1 cells by increasing PPAR-γ expression. Therefore, our results showed that 6:2 Cl-PFESA has the potential to induce liver damage and dysfunction in female mice, and this effect was achieved through PPAR-γ. This study is the first to reveal the hepatic toxicity of 6:2 Cl-PFESA in female mammals and provides new insights for subsequent in-depth research.

Maternal Polystyrene Microplastic Exposure during Gestation and Lactation Altered Metabolic Homeostasis in the Dams and Their F1 and F2 Offspring.

Microplastics (MPs) are considered as a pollutant of marine environments and have become a global environmental problem in recent years. A number of studies have demonstrated that MPs can enter the human food chain, and MPs have even been detected in human stools. Therefore, there is increasing concern about the potential risks of MPs to human and animal health. Here, we investigated maternal polystyrene MPs exposure during gestation and lactation and evaluated the potential effects on dams and the F1 (both PND 42 and 280) and F2 (PND 42) generations. The results of transcriptome and 16S rRNA sequencing indicated that MPs caused the metabolic disorder in maternal MPs associated with gut microbiota dysbiosis and gut barrier dysfunction. Simultaneously, maternal MPs exposure also had the intergenerational effects and even caused long-term metabolic consequences in the F1 and F2 generations. In addition, in F1 (PND 42), the composition of gut microbiota did not change significantly, while the hepatic transcriptome and serum metabolite changes showed the potential risk in metabolic disorder. Then, the potential of hepatic lipid accumulation was observed in adult F1 mice (PND 280), especially in the female mice. Our results demonstrated that maternal MPs exposure during gestation and lactation increases the risk of metabolic disorder, and these results provide new insight into the potential long-term hazards of MPs.

Subchronic exposure of environmentally relevant concentrations of F-53B in mice resulted in gut barrier dysfunction and colonic inflammation in a sex-independent manner.

F-53B (6:2 chlorinated polyfluorinated ether sulfonate) is currently recognized as a safe alternative to long-chain PFASs in China. However, an increasing number of studies have recently authenticated its biotoxicological effects. In this study, for evaluating the gut toxicity of F-53B in mammals, both female and male mice were orally exposed to 0, 1, 3, or 10 µg/L F-53B for 10 weeks. Our results showed that F-53B significantly accumulated in the colon, ileum and serum when exposed to 10 µg/L F-53B for 10 weeks. F-53B exposure not only increased the transcriptional levels of ion transport-related genes but could also interact with the CFTR protein directly. Interestingly, subchronic F-53B exposure also increased the transcription of mucus secretion-related genes, but the protein level of Muc2 decreased after F-53B exposure, indicating that there was a compensatory phenomenon after mucus barrier injury. Furthermore, F-53B exposure also induced colonic inflammation associated with gut microbiota dysbiosis in the colon. Taken together, our results indicated that the potential gut toxicity of F-53B and almost all of the changed parameters were significantly affected in both female and male mice, suggesting that F-53B could disturb the gut barrier without sex dependence in mice.

Gut microbiota: An underestimated and unintended recipient for pesticide-induced toxicity.

Pesticide pollution residues have become increasingly common health hazards over the last several decades because of the wide use of pesticides. The gastrointestinal tract is the first physical and biological barrier to contaminated food and is therefore the first exposure site. Interestingly, a number of studies have shown that the gut microbiota plays a key role in the toxicity of pesticides and has a profound relationship with environmental animal and human health. For instance, intake of the pesticide of chlorpyrifos can promote obesity and insulin resistance through influencing gut and gut microbiota of mice. In this review, we discussed the possible effects of different kinds of widely used pesticides on the gut microbiota in different experimental models and analyzed their possible subsequent effects on the health of the host. More and more studies indicated that the gut microbiota of animals played a very important role in pesticides-induced toxicity, suggesting that gut micriobita was also the unintended recipient of pesticides. We hope that more attention can focus on the relationship between pesticides, gut microbiota and environmental health risk assessment in near future.

Short-term propamocarb exposure induces hepatic metabolism disorder associated with gut microbiota dysbiosis in adult male zebrafish.

Propamocarb (PM) is a pesticide that is widely used to protect cucumbers and other plants from downy mildew. Recently, some studies indicated that PM exposure had potential toxic effects in animals. In this study, adult male zebrafish were exposed to 100 and 1000 µg/l PM for 7 days to assess its effects on metabolism and the gut microbiota. We observed a significant decrease in triglyceride (TG) in the livers of zebrafish that were exposed to 1000 µg/l PM for 7 days. At the same time, some genes related to glycolysis and lipid metabolism in the livers of zebrafish, including hexokinase-1 (HK1), pyruvate kinase (PK), acyl-CoA oxidase (Aco), peroxisome proliferator activated receptor alpha (Ppar-α), apolipoprotein A-IV-like (Apo), Acetyl CoA carboxylase-1 (Acc1), diacylglycerol acyltransferase (Dgat), and fatty acid synthase (Fas), were also decreased significantly after PM exposure. Based on GC-MS metabolomics analysis, a total of 48 metabolites changed significantly in the 1000 µg/l PM treatment group in comparison with the control group. These altered metabolites were mainly associated with the glycolysis, amino acid metabolism, and lipid metabolism pathways. Interestingly, we further found that the 1000 µg/l PM treatment group also showed significant elevations in Proteobacteria, Bacteroidetes, and Firmicutes at the phylum level. Sequencing of the 16S rRNA gene in the V3-V4 region also showed a significant change in the abundance and diversity of the gut microbiota in the 1000 µg/l PM treatment group. Our results indicated that exposure to PM for a short time could induce hepatic metabolic disorders and gut microbiota dysbiosis in adult male zebrafish.

Modification of chitin with high adsorption capacity for methylene blue removal.

Porous chitin sorbents (PChs) with different content of chitin, ranging from 0.9% to 3.5%, were prepared by gel method with CaBr2·xH2O/CH3OH solution and characterized by FT-IR, XRD and SEM. The adsorption isotherms and kinetic analysis of methylene blue (MB) onto PChs were studied. Experimental results illustrated lower crystallinity and more pores of PChs containing 3.5% chitin displayed higher adsorption capacity, the removal of MB was 79.8%. The adsorption equilibrium isotherm curve of MB onto PChs adsorbents conformed to the Freundlich equation. The PFO, PSO and Weber-Morris models were applied to fit with the adsorption kinetics. The results demonstrated the adsorption of MB might be the mass transfer of heterogeneous system and involve multiple diffusion steps. The adsorption capacity of PChs with 3.5% chitin can maintain 65% removal ratio of MB after being used six adsorption-desorption cycles. It was supposed that PChs may be a promising, cheap, environmentally friendly and efficient adsorbent for some dye wastewater treatment in the near future.

Chronic exposure to low concentrations of lead induces metabolic disorder and dysbiosis of the gut microbiota in mice.

Lead (Pb) is one of the most prevalent toxic, nonessential heavy metals that can contaminate food and water. In this study, effects of chronic exposure to low concentrations of Pb on metabolism and gut microbiota were evaluated in mice. It was observed that exposure of mice to 0.1mg/L Pb, supplied via drinking water, for 15weeks increased hepatic TG and TCH levels. The levels of some key genes related to lipid metabolism in the liver increased significantly in Pb-treated mice. For the gut microbiota, at the phylum level, the relative abundance of Firmicutes and Bacteroidetes changed obviously in the feces and the cecal contents of mice exposed to 0.1mg/L Pb for 15weeks. In addition, 16s rRNA gene sequencing further discovered that Pb exposure affected the structure and richness of the gut microbiota. Moreover, a 1H NMR metabolic analysis unambiguously identified 31 metabolites, and 15 metabolites were noticeably altered in 0.1mg/L Pb-treated mice. Taken together, the data indicate that chronic Pb exposure induces dysbiosis of the gut microbiota and metabolic disorder in mice. CAPSULE: Chronic Pb exposure induces metabolic disorder, dysbiosis of the gut microbiota and hepatic lipid metabolism disorder in mice.

Polystyrene microplastics induce microbiota dysbiosis and inflammation in the gut of adult zebrafish.

Microplastic (MP) are environmental pollutants and have the potential to cause varying degrees of aquatic toxicity. In this study, the effects on gut microbiota of adult male zebrafish exposed for 14 days to 100 and 1000 µg/L of two sizes of polystyrene MP were evaluated. Both 0.5 and 50 µm-diameter spherical polystyrene MP increased the volume of mucus in the gut at a concentration of 1000 µg/L (about 1.456 × 1010 particles/L for 0.5 µm and 1.456 × 104 particles/L for 50 µm). At the phylum level, the abundance of Bacteroidetes and Proteobacteria decreased significantly and the abundance of Firmicutes increased significantly in the gut after 14-day exposure to 1000 µg/L of both sizes of polystyrene MP. In addition, high throughput sequencing of the 16S rRNA gene V3-V4 region revealed a significant change in the richness and diversity of microbiota in the gut of polystyrene MP-exposed zebrafish. A more in depth analysis, at the genus level, revealed that a total of 29 gut microbes identified by operational taxonomic unit (OTU) analysis were significantly changed in both 0.5 and 50 µm-diameter polystyrene MP-treated groups. Moreover, it was observed that 0.5 µm polystyrene MP not only increased mRNA levels of IL1α, IL1ß and IFN but also their protein levels in the gut, indicating that inflammation occurred after polystyrene MP exposure. Our findings suggest that polystyrene MP could induce microbiota dysbiosis and inflammation in the gut of adult zebrafish.

Insights Into a Possible Influence on Gut Microbiota and Intestinal Barrier Function During Chronic Exposure of Mice to Imazalil.

The fungicide imazalil (IMZ) is widely used to prevent and treat fungal diseases in plants and animals. Here, male adult C57BL/6 mice were exposed to 0.1, 0.5, and 2.5 mg/kg body weight IMZ for 2, 5, or 15 weeks. The microbiota in cecal contents and feces changed during chronic IMZ exposure at phylum and genus levels. Sequencing of the V3-V4 region of the bacterial 16S rRNA gene revealed a significant change in the richness of microbiota in cecal contents and feces after exposure to 2.5 mg/kg IMZ for 15 weeks. Operational taxonomic unit (OTU) analysis indicated that 31.1% of cecal OTUs and 14.0% of fecal OTUs changed after IMZ exposure. In addition, chronic IMZ exposure also disturbed the intestinal barrier function of the mice, reducing mucus secretion, decreasing the expression of cystic fibrosis transmembrane conductance regulator (CFTR)-related genes in both the ileum and colon. Molecular docking analysis revealed that key hydrogen bonds were formed by nitrogen atoms of the imidazole bond with Val440 of CFTR and Ala697 of the SLC26 family. Our data suggested that gut microbiota and intestinal barrier were potential toxicological targets of IMZ.

Imazalil exposure induces gut microbiota dysbiosis and hepatic metabolism disorder in zebrafish.

The fungicide imazalil (IMZ) is used extensively to preserve freshness, prevent decay and control fungal infections in fruits, vegetables or other plants. Recently, some studies have reported that the real in aquatic systems have reached very high levels. Here, male adult zebrafish were exposed to 100 and 1000µg/L IMZ for 1, 7, 21days, and the gut microbiota and hepatic metabolism were evaluated. Exposure to a high concentration of IMZ for 21days decreased mucin secretion in the gut. Sequencing of the V3-V4 region of the bacterial 16S rRNA gene revealed a significant increase in the diversity of gut microbiota in male zebrafish. At the phylum level, the composition of Proteobacteria and Bacteroidetes was decreased, while those Fusobacteria and Firmicutes increased in the gut after exposure to 1000µg/L IMZ for 21days. At the genus level, 29 species of microorganisms were significantly changed after IMZ exposure. Based on GC/MS metabolomics analysis, 101 metabolites were observably significantly altered in the 1000µg/L IMZ-treatment group. These changed metabolites were mainly associated with the pathway of glycolysis, amino acid metabolism, and lipid metabolism. In addition, the transcription of some genes related to glycolysis and lipid metabolism, including Aco, Cpt1, Acc1, Srebp1a and Fas, was decreased significantly in the liver of zebrafish when exposed to 100 and 1000µg/L IMZ for 7 or 21days. These results indicated that exposure to IMZ could cause gut microbiota dysbiosis and metabolic disorders in adult zebrafish.

(2-Acetyl-phenolato)(2,2'-bipyridine)nitratocopper(II).

In the title compound, [Cu(C(8)H(7)O(2))(NO(3))(C(10)H(8)N(2))], the Cu(II) ion is five-coordinate in a distorted square-pyramidal geometry. The basal positions are occupied by two N atoms from a 2,2'-bipyridine ligand and two O atoms from the 2-acetyl-phenolate anion. The axial position is occupied by one O atom of a nitrate anion. In the bipyridine ligand, the two pyridine rings are slightly twisted by an angle of 3.5 (1)°. The crystal structure is stabilized by C-H⋯O hydrogen bonds.

Determination of proteins at nanogram levels with Bordeaux red based on the enhancement of resonance light scattering.

A simple, sensitive and selective method was proposed for the determination of proteins by using a resonance light scattering technique. The weak resonance light scattering (RLS) of Bordeaux red (BR) can be enhanced greatly in the pH range 3.87-3.96 by the addition of micro amounts of proteins, resulting in four characteristic peaks in the wavelength range 250-600 nm. At the maximal wavelength of 363 nm, the enhanced RLS is proportional to the concentration of proteins in the range 0.12-10.8 microg ml-1 for bovine serum albumin (BSA) and 0.24-18.0 microg ml-1 for human serum albumin (HSA). The detection limits were 40.0 and 52.9 ng ml-1 for BSA and HSA, respectively. The present method has been applied to the determination of total proteins in human serum, urine and saliva samples. The obtained results are in good agreement with those obtained by the Bradford method with relative standard deviations (R.S.D.) of 0.9-2.3%.

[Studies on the interaction between thionine and deoxyribo-nucleic acid by ethidium bromide probe].

The interaction between thionine and deoxyribonucleic acid was studied with ethidium bromide probe in Tris-HCl buffer solution at pH 7.4 by fluorescence spectra, electronic absorption spectra, and resonance light scattering spectra. From the obtained results, it was found obviously that the planar structure of thionine can be intercalated into the stacked base pairs of DNA, which is the major controlling factor. The binding constant was found to be 1.0 x 10(5) L x mol(-1).

Determination of trace proteins with pyronine Y and SDS by resonance light scattering.

A new resonance light scattering (RLS) probe for determining proteins is presented. The weak RLS of pyronine Y-SDS can be enhanced substantially by adding proteins in the presence of H2SO4, resulting in a strong and wide RLS band in the region 310-425 nm. The interaction of pyronine Y-SDS with proteins was studied on the basis of this behavior and a new quantitative method was developed for determining proteins. The enhanced RLS intensity is proportional to the concentration of proteins in the range 0.15-3.6 microg mL(-1) for bovine serum albumin (BSA) and 0.06-4.8 microg mL(-1) for human serum albumin (HSA), with detection limits of 21.0 and 12.0 ng mL(-1), respectively. This method is characterized by high sensitivity, rapidity of reaction, and simplicity. Four synthetic samples were determined satisfactorily and recovery was 99.5-101.5%. Results for human serum and urine samples were in agreement with those obtained by the Bradford method, with relative standard deviations (RSD) of 1.5-3.1%.