Microcystin-LR (MC-LR) and microcystin-RR (MC-RR) are the two most common microcystins (MCs) present in fresh water posing a direct threat to public health because of their hepatotoxicity. A novel MC-degrading bacterium designated MC-LTH1 capable of degrading MC-LR and -RR was isolated, and the degradation rates and mechanisms of MC-LR and -RR for this bacterium were investigated. The bacterium was identified as Bordetella sp. and shown to possess a homologous mlrA gene responsible for degrading MCs. To the best of our knowledge, this is the first report of mlrA gene detection in Bordetella species. MC-LR and -RR were completely degraded separately at rates of 0.31 mg/(L h) and 0.17 mg/(L h). However, the degradation rates of MC-LR and -RR decreased surprisingly to 0.27 mg/(L h) and 0.12 mg/(L h), respectively, when both of them were simultaneously present. Degradation products were identified by high performance liquid chromatography coupled with time-of-flight mass spectrometry. Adda (m/z 332.2215, C20H29NO3) commonly known as a final product of MC degradation by isolated bacteria was detected as an intermediate in this study. Linearized MC-LR (m/z 1013.5638, C49H76N10O13), linearized MC-RR (m/z 1056.4970, C49H77N13O13), and tetrapeptide (m/z 615.3394, C32H46N4O8) were also detected as intermediates. These results indicate that the bacterial strain MC-LTH1 is quite efficient for the detoxification of MC-LR and MC-RR, and possesses significant bioremediation potential.

This study aimed to determine the most significant molecular features associated with the liver specificity of the carcinogenicity of N-nitroso compounds (NOCs). Accordingly, quantitative structure–activity relationship (QSAR) analysis was performed to extract molecular information from NOCs using a topological substructural molecular descriptor (TOPS-MODE) approach. A linear discriminant analysis (LDA) model of a series of NOCs for rat liver was developed using TOPS-MODE descriptors to predict nonliver- and liver-carcinogenic NOCs. Two descriptors exclusively calculated from the molecular structures of the compounds were selected by a genetic algorithm. The descriptors were then weighted with bond distances as well as the Abraham solute descriptor partition between water and aqueous solvent systems to indicate the importance of their roles in liver specificity. The performances of the LDA model were rigorously validated by leave-one-out cross-validation and external validation, with the prediction accuracy reaching 88.3% and 80.0%, respectively. The contributions of the different molecular fragments to rat-liver specificity were computed. The results served as important information related to liver specificity and were analyzed from the chemical–molecular perspective. The resulting model can provide an efficient method to discriminate between as well as extrapolate nonliver- and liver-carcinogenic NOCs. The contribution of the entire nitrosamine molecule was determined as being responsible for the liver specificity of nitrosamine carcinogenicity. Although the QSAR showed limitations in complex hepatocarcinogenicity, the proposed method may considerably help elucidate the role of nitrosamines in liver specificity from the chemical–molecular perspective. The nature of these enzyme–substrate interactions is characterized. Insight into the chemical–structural and biological factors related to the liver-specific biological activity of NOCs is also provided.

A linear discriminant analysis (LDA) coupled with an enhanced replacement method (ERM) was used as an alternative method to predict the carcinogenicity of N-nitroso compounds (NOCs) in rats. This presented LDA based on the topological substructural molecular descriptors (TOPS-MODE) approach was developed to predict the carcinogenic and noncarcinogenic activity on a data set of 111 NOCs with a good classification value of 90.1%. The predictive power of the LDA model was validated through an external validation set (37 compounds) with a prediction accuracy of 94.6% and a leave-one-out cross-validation procedure (LOOCV) with a good prediction of 86.5%. This methodology showed that the TOPS-MODE descriptors weighted, respectively, by bond dipole moment and Abraham solute descriptor dipolarity/polarizability affected the NOC carcinogenicity. The contributions of certain bonds and fragments to carcinogenicity were used to assess biotransformation and carcinogenic mechanisms. The positive contribution of the carbon–nitrogen single bond (between the N-nitroso group and α-carbon to the N-nitroso group) indicated that the α-hydroxylation reaction could occur at the α-carbon or otherwise not occur. Similarly, the contributions from the molecular fragment could be applied to indicate whether the fragments generated an alkylating agent. These results suggested that this approach could discriminate between carcinogenic and noncarcinogenic NOCs, thereby providing insight into the structural features and chemical factors related to NOC carcinogenicity.

ObjectiveTo report the prevalence and trend of overweight and obesity among students aged 7-22 years in Jiangsu, 2010 to 2013.MethodsThis cross-sectional study was carried out as part of students physical fitness and health survey in Jiangsu province. A total of 255,581 subjects (50.03% males and 49.97% females) enrolled in 82 school and 10 universities in Jiangsu. Weights and heights were obtained for each subject and its body mass index (BMI) was calculated using the Chinese Working Group on Obesity in China (CWGO).ResultsAnthropometric measurement including bodyweight, height, BMI and bust were significantly different between males in urban compared to females living rural areas (P<0.001). The total prevalence of overweight and obesity was 12.4% and 5.7%. Males had a significantly higher rate than in female's student. The prevalence of overweight and obesity by age groups was (14.5%, 10.3%) at age 7-11 years, (11.2%, 6.8%) at age 12-14 years, (11.7%, 3.1%) at age 15-17 years, and (11.4%, 2.3%) at age 18-22 years. By regions; the highest prevalence of overweight obesity reported in Taizhou (10%, 14.2%), Xuzhou (9.4%, 12.5%), and Nanjing (9.2%, 15.6%), respectively.ConclusionThe finding declares that overweight and obesity are important health problems among students in Jiangsu Province. Early intervention programme are needed to address this problems.

ObjectiveCytochrome P450 2E1 (CYP2E1) is an important metabolizing enzyme involved in oxidative stress responses to benzene, a chemical associated with bone marrow toxicity and leukemia. We aimed to identify the CYP2E1 genetic biomarkers of susceptibility to benzene toxicity in support of environmental and occupational exposure prevention, and to test whether a model using immortal human lymphocytes might be an efficient tool for detecting genetic biomarkers.MethodsImmortalized human lymphocyte cell lines with independent genotypes on four CYP2E1 SNP sites were induced with 0.01% phenol, a metabolite of benzene. CYP2E1 gene function was evaluated by mRNA expression and enzyme activity. DNA damage was measured by Single-Cell Gel Electrophoresis (SCGE).ResultsAmong the four SNPs, cells with rs2070673TT and rs2030920CC showed higher levels of CYP2E1 transcription and enzymatic activity than the other genotypes in the same SNP site. Cells with higher gene expression genotypes also showed higher comet rates compared with lower gene expression genotypes.ConclusionThese results suggest that CYP2E1 rs2070673 and rs2030920 might be the genetic biomarkers of susceptibility to benzene toxicity and that the immortalized human lymphocytes model might be an efficient tool for the detection of genetic biomarkers of susceptibility to chemicals.

ObjectiveTo isolate and characterize indigenous algicidal bacteria and their algae-lysing compounds active against Microcystis aeruginosa, strains TH1, TH2, and FACHB 905.MethodsThe bacteria were identified using the Biolog automated microbial identification system and 16S rDNA sequence analysis. The algae-lysing compounds were isolated and purified by silica gel column chromatography and reverse-phase high performance liquid chromatography. Their structures were confirmed by Nuclear Magnetic Resonance (NMR) and Fourier Transform Infrared (FT-IR) spectroscopy. Algae-lysing activity was observed using microscopy.ResultsThe algae-lysing bacterium LTH-2 isolated from Lake Taihu was identified as Serratia marcescens. Strain LTH-2 secreted a red pigment identified as prodigiosin (C20H25N3O), which showed strong lytic activity with algal strains M. aeruginosa TH1, TH2, and FACHB 905 in a concentration-dependent manner. The 50% inhibitory concentration (IC50) of prodigiosin with the algal strains was 4.8 (±0.4)×10−2 μg/mL, 8.9 (±1.1)×10−2 μg/mL, and 1.7 (±0.1)×10−1 μg/mL in 24 h, respectively.ConclusionThe bacterium LTH-2 and its pigment had strong Microcystis-lysing activity probably related to damage of cell membranes. The bacterium LTH-2 and its red pigment are potentially useful for regulating blooms of harmful M. aeruginosa.

ObjectiveThis study aims to investigate and compare the toxic effects of four types of metal oxide (ZnO, TiO2, SiO2, and Al2O3) nanoparticles with similar primary size (∼20 nm) on human fetal lung fibroblasts (HFL1) in vitro.MethodsThe HFL1 cells were exposed to the nanoparticles, and toxic effects were analyzed by using MTT assay, cellular morphology observation and Hoechst 33 258 staining.ResultsThe results show that the four types of metal oxide nanoparticles lead to cellular mitochondrial dysfunction, morphological modifications and apoptosis at the concentration range of 0.25-1.50 mg/mL and the toxic effects are obviously displayed in dose-dependent manner. ZnO is the most toxic nanomaterials followed by TiO2, SiO2, and Al2O3 nanoparticles in a descending order.ConclusionThe results highlight the differential cytotoxicity associated with exposure to ZnO, TiO2, SiO2, and Al2O3 nanoparticles, and suggest an extreme attention to safety utilization of these nanomaterials.

•ALCAR partially alleviated benzene-induced hematotoxicity.•ALCAR reduced benzene-induced oxidative stress.•ALCAR decreased DNA damage in benzene exposure mice.Benzene is an environmental pollutant and occupational toxicant which induces hematotoxicity. Our previous metabonomics study suggested that acetyl-l-carnitine (ALCAR) decreased in the mouse plasma and bone marrow (BM) cells due to benzene exposure. In the present study, the topic on whether ALCAR influences hematotoxicity caused by benzene exposure was explored. Thirty-two male C3H/He mice were divided into four groups: control group (C: vehicle, oil), benzene group (150 mg/kg body weight (b.w.) benzene), benzene + A1 group (150 mg/kg b.w. benzene + 100 mg/kg b.w. ALCAR), and benzene + A2 group (150 mg/kg b.w. benzene + 200 mg/kg b.w. ALCAR). Benzene was injected subcutaneously, and ALCAR was orally administrated via gavage once daily for 4 weeks consecutively. After the experimental period, the blood routine, BM cell number and frequency of hematopoietic stem/progenitor cell (HS/PC) were assessed. The mitochondrial membrane potential and ATP level were determined to evaluate the mitochondrial function. Reactive oxygen species (ROS), hydrogen peroxide (H2O2) and malondialdehyde (MDA) levels were also examined, and the comet assay was performed to measure oxidative stress. Results showed that ALCAR intervention can partially reduce the benzene-induced damage on BM and HS/PCs and can simultaneously alleviate the DNA damage by reducing benzene-induced H2O2, ROS, and MDA.

•The cytotoxicity of three different MWCNTs was investigated.•Oxidative stress and inflammation were increased by raw MWCNTs and MWCNTs–COOH.•The physicochemical properties of MWCNTs lead to an increased bioactivity.•The mechanism of toxicity may involve the activation of the MAPK and NF-κB pathways.Carbon nanotubes (CNTs) are widely used in industry and biomedicine. While several studies have focused on biological matters, attempts to systematically elucidate the toxicity mechanisms of CNTs are limited. The aim of the present study was to evaluate and compare the cytotoxicity of raw multi-walled carbon nanotubes (MWCNTs) and MWCNTs functionalized with carboxylation (MWCNTs–COOH) or polyethylene glycol (MWCNTs–PEG) in murine macrophages. Our results show that only MWCNTs–COOH and raw MWCNTs alter the oxidative potential of macrophages by increasing reactive oxygen species and the expression of pro-inflammatory factors in both a concentration- and surface coating-dependent manner. The data suggest that compare with raw MWCNTs and MWCNTs–PEG, the MWCNTs–COOH produces a significant increase in ROS generation, interruption of ATP synthesis, and activation of the MAPK and NF-κB signaling pathways, which in turn upregulates IL-1β, IL-6, TNF-α, and iNOS to trigger cell death. These findings suggest that contributory cellar uptake caused by physicochemical factors rather than residual metal catalysts plays a role in ROS-mediated pro-inflammatory responses in vitro.