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Dechlorane 602 (Dec 602), a chlorinated flame retardant, has been widely detected in different environmental matrices and biota. However, toxicity data for Dec 602 seldom have been reported. A metabolomics study based on ultra-high performance liquid chromatography coupled with ion trap time-of-flight mass spectrometry was employed to study the urine and sera metabolic profiles of mice administered with Dec 602 (0, 0.001, 0.1, and 10 mg/kg body weight per day) for 7 days. A significant difference in metabolic profiling was observed between the Dec 602 treated group and the control group by multivariate analysis, which directly reflected the metabolic perturbations caused by Dec 602. The metabolomics analyses of urine from Dec 602-exposed animals exhibited an increase in the levels of thymidine and tryptophan as well as a decrease in the levels of tyrosine, 12,13-dihydroxy-9Z-octadecenoic acid, 2-hydroxyhexadecanoic acid and cuminaldehyde. The metabolomics analyses of sera showed a decrease in the levels of kynurenic acid, daidzein, adenosine, xanthurenic acid and hypoxanthine from Dec 602-exposed animals. These findings indicated Dec 602 induced disturbance in phenylalanine, tyrosine and tryptophan biosynthesis, tryptophan metabolism, tyrosine metabolism, pyrimidine metabolism, purine metabolism, ubiquinone and other terpenoid-quinone biosynthesis; phenylalanine metabolism and aminoacyl-tRNA biosynthesis. Significant alterations of immune and neurotransmitter-related metabolites (tyrosine, tryptophan, kynurenic acid, and xanthurenic acid) suggest that the toxic effects of Dec 602 may contribute to its interactions with the immune and neuronal systems. This study demonstrated that the UHPLC-ESI-IT-TOF-MS-based metabolomic approach can obtain more specific insights into the potential toxic effects of Dec 602 at molecular level.

Tobacco (Nicotiana tabacum) is one of the most widely cultivated commercial non-food crops with significant social and economic impacts. Here we profiled transcriptome and metabolome from 54 tobacco samples (2–3 replicates; n = 151 in total) collected from three varieties (i.e. genetic factor), three locations (i.e. environmental factor), and six developmental stages (i.e. developmental process). We identified 3,405 differentially expressed (DE) genes (DEGs) and 371 DE metabolites, respectively. We used quantitative real-time PCR to validate 20 DEGs, and confirmed 18/20 (90%) DEGs between three locations and 16/20 (80%) with the same trend across developmental stages. We then constructed nine co-expression gene modules and four co-expression metabolite modules , and defined seven de novo regulatory networks, including nicotine- and carotenoid-related regulatory networks. A novel two-way Pearson correlation approach was further proposed to integrate co-expression gene and metabolite modules to identify joint gene–metabolite relations. Finally, we further integrated DE and network results to prioritize genes by its functional importance and identified a top-ranked novel gene, LOC107773232, as a potential regulator involved in the carotenoid metabolism pathway. Thus, the results and systems-biology approaches provide a new avenue to understand the molecular mechanisms underlying complex genetic and environmental perturbations in tobacco.

Multihole ZnO hierarchical architectures were prepared by tartaric acid assisted hydrothermal synthesis, TA acts as a capping agent and structure-directing agent during the synthesis. Hydrazine acts as alkali source. XRD confirmed that that all ZnO possess the hexagonal wurtzite structure, and the crystalline of the sample turns better after annealed. The PL spectra can be tuned by changing TA concentration. The FTIR spectra of ZnO nanostructures shows the main absorbance peaks of all samples are located at about 547 cm−1, which are attributed to the vibrations of elongation of ZnO without any other bonds.

Epidemiological and animal studies indicate that increased exposure to bisphenol A (BPA) induces various human cardiovascular diseases (CVDs), including myocardial infarction, arrhythmias, dilated cardiomyopathy, atherosclerosis, and hypertension. Bisphenol S (BPS), an alternative to BPA, is increasingly present in various consumer products and human bodies worldwide. Recently, emerging evidence has shown that BPS might be related to cardiovascular disorders. In this review, we present striking evidence of the correlation between BPA exposure and various CVDs, and show that a nonmonotonic dose-response curve (NMDRC) was common in studies of the CV effects of BPA in vivo. The CV impairment induced by low doses of BPA should be highlighted, especially during developmental exposure or during coexposure with other risk factors. Furthermore, we explored the possible underlying mechanisms of these effects-particularly nuclear receptor signaling, ion channels, and epigenetic mechanisms-and the possible participation of lipid metabolism, oxidative stress and cell signaling. As the potential risks of BPA exposure in humans are still noteworthy, studies of BPA in CVDs should be strengthened, especially with respect to the mechanisms, prevention and treatment. Moreover, the potential CV risk of BPS reported by in vivo studies calls for immediate epidemiological investigations and animal studies to reveal the relationships of BPS and other BPA alternatives with human CVDs.

Acetylcholinesterase (AChE, EC 3.1.1.7) is a classical biomarker for monitoring contamination and intoxication of organophosphate (OP) and carbamate pesticides. In addition to these classical environmental AChE inhibitors, other organic toxic substances have been found to alter AChE activity in various species. These emerging organic AChE disruptors include certain persistent organic pollutants (POPs), polycyclic aromatic hydrocarbons (PAHs), and wildly used chemicals, most of which have received considerable public health concern in recent years. It is necessary to re-evaluate the environmental significances of AChE in terms of these toxic substances. Therefore, the present review is aiming to summarize correlations of AChE activity of certain organisms with the level of the contaminants in particular habitats, disruptions of AChE activity upon treatment with the emerging disruptors in vivo and in vitro, and action mechanisms underlying the effects on AChE. Over 40 chemicals belonging to six main categories were reviewed, including 12 POPs listed in the Stockholm Convention. AChE activity in certain organisms has been found to be well correlated with the contamination level of certain persistent pesticides and PAHs in particular habitats. Moreover, it has been documented that most of the listed toxic chemicals could inhibit AChE activity in diverse species ranging from invertebrates to mammals. Besides directly inactivating AChE, the mechanisms in terms of interference with the biosynthesis have been recognized for some emerging AChE disruptors, particularly for dioxins. The collected evidence suggests that AChE could serve as a potential biomarker for a diverse spectrum of organic environmental pollutants.

Peroxisome proliferator-activated receptors (PPARs) play vital roles in cardiovascular pathophysiology, such as energy balance, cell proliferation/apoptosis, inflammatory response, and adipocyte differentiation. These vital roles make PPARs potential targets for therapeutic prevention of cardiovascular diseases (CVDs). Emerging evidence indicates that the crosstalk of microRNAs (miRNAs) and PPARs contributes greatly to CVD pathogenesis. PPARs are inhibited by miRNAs at posttranscriptional mechanisms in the progress of pulmonary hypertension and vascular dysfunction involving cell proliferation/apoptosis, communication, and normal function of endothelial cells and vascular smooth muscle cells. In the development of atherosclerosis and stroke, the activation of PPARs could change the transcripts of target miRNA through miRNA signalling. Furthermore, the mutual regulation of PPARs and miRNAs involves cell proliferation/apoptosis, cardiac remodeling, and dysfunction in heart diseases. In addition, obesity, an important cardiovascular risk, is modulated by the regulatory axis of PPARs/miRNAs, including adipogenesis, adipocyte dysfunction, insulin resistance, and macrophage polarization in adipose tissue. In this review, the crosstalk of PPARs and miRNAs and their emerging regulatory roles are summarized in the context of CVDs and risks. This provides an understanding of the underlying mechanism of the biological process related to CVD pathophysiology involving the interaction of PPARs and miRNAs and will lead to the development of PPARs/miRNAs as effective anti-CVD medications.

The hepatopancreatic cell culture of the kuruma prawn, Litopenaeusvannamei, was conducted to identify the effects of zinc on cell division. The culturesystem consists of medium 199 (M 199) supplemented with 0.060 mol/L NaCl,1.011g/L glucose, 1000 UI/ml penicillin, 1000 μg/ml treptomycin, 20% heatinactivated fetal calf serum (FCS) for primary cells and 10 % for subculture cells. TheRNA/DNA ratio in cultured cells was measured. The results show that the celldivision of cultured hepatopancreas cells in L. vannamei was increased by the optimalconcentration of Zn2+, 80 μg/L.

The equilibria phase of the ternary systems NaCl-CsCl-H2O was studied at 50°C by the isothermal evaporation method. The equilibrium phase diagrams were plotted in line with the experimental data. It suggest that the phase diagram of NaCl-CsCl-H2O is the simple eutectic type where one invariant point is found to have the compositions of 12.3% NaCl, 54.1% CsCl and 33.6% H2O by mass, respectively. The study provide fundamental thermodynamic data of brine system that contains sodium and cesium, and has practical significance for the brine’s comprehensive utilization.

With the widely research of Photocatalytic titanium dioxide, researchers have found another way of managing air quality. As an excellent photocatalyst material, nanometer titanium dioxide has begun to be used in road engineering in recent years. In this paper, at first, different content of titanium dioxide were dispersed evenly and separately in a kind of silane solvent to make the coating material with photocatalytic performance. The results show that nanometer titanium dioxide is able to decompose CO, HC, NO and CO2 after being dispersed in silane solvent. The results also show that a certain content oftitanium dioxide can be chosen after considering effect, workability and economic factors in practical application. Then the brushing method and the decomposition effect of the photocatalytic paint are discussed. The tests indicate that proper content of nanometer titanium dioxide with suitable brushing method can maximize catalytic efficiency. At last, in order to study the decomposition mechanism, using ion chromatography and chemical titration to analyze the decomposition products separately, the results prove that nanometer titanium dioxide can decompose NO, HC, CO and other harmful gases into nitrate and carbonate.

With the widely research of nano-TiO2, researchers have found another way of managing air quality. As an excellent photocatalyst material, nanometer titanium dioxide has begun to be used in road engineering in recent years. In this paper, substantial gas decomposition tests are performed utilizing the self-designed sealed container and UV aging box. At first, the catalytic efficiencies of nanometer titanium dioxide dispersed in silane solvent and in asphalt mixture were compared. The results show that nanometer titanium dioxide is able to decompose CO, HC and NO after being dispersed in silane solvent and asphalt mixture. To achieve the same catalytic efficiency, the amount of the nanometer titanium dioxide dispersed in silane solvent is much less than that in asphalt mixture. For asphalt mixture, high void fraction may mean high catalytic efficiency. Then the long-term decomposition of asphalt mixture was discussed. The asphalt mixture still has good catalytic decomposition effect after six months. The catalytic effect of asphalt mixture does not diminish over time and the effect of decomposing HC has improved after six months. At last, for cement paint, the catalytic effect of decomposing NO and HC does not diminish over time, but the effect of decomposing CO reduces.

Studies have shown that nanometer Titanium dioxide is an excellent photocatalyst material, which owns environmental protection function of decomposing car exhaust, and it begins to be used in road works in recent years. In this paper, firstly a representative concentration ratio of each component in exhaust gas is reached according to statistical result from a large number of vehicle exhaust samples, and simulated gas used in laboratory test is prepared according to the ratio. Then substantial gas- decomposition tests are performed utilizing the self-designed sealed container and UV aging box. Applying ion chromatography to analyze the decomposition products, it is proved that nano-titanium dioxide can decompose NOx, HC, CO and other harmful gases into nitrate and carbonate. Subsequently, an excellent concrete protection materials- anticorrosive of silane solvent is selected as dispersion solvent, and a certain amount of titanium dioxide is dispersed evenly in the solvent to make the coating material with photocatalytic performance, the brushing method and decomposition effect of the coating material are discussed. In the end, a brushing method with better decomposition effect is applied on cement collision wall on middle ring in Pudong district, while nano-titanium is also contained in the surface layer of pavement; Field measurement results show that the decomposition of car exhaust effect is obvious.

Aryl hydrocarbon receptor (AhR), a ligand-dependent nuclear receptor, is involved in a diverse spectrum of biological and toxicological effects. Due to the lack of three dimensional (3D) crystal or nuclear magnetic resonance structure, the mechanisms of these complex effects of AhR remain to be unclear. Also, commercial monoclonal antibodies (mAbs) against human AhR protein (hAhR), as alternative immunological tools, are very limited. Thus, in order to provide more tools for further studies on hAhR, we prepared two mAbs (1D6 and 4A6) against hAhR. The two newly generated mAbs specifically bound to amino acids 484-508 (located in transcription activation domain) and amino acids 201-215 (located in Per-ARNT-Sim domain) of hAhR, respectively. These epitopes were new as compared with those of commercial mAbs. The mAbs were also characterized by enzyme-linked immunosorbent assay, western blot, immunoprecipitation and indirect immunofluorescence assay in different cell lines. The results showed that the two mAbs could recognize the linearized AhRs in six different human cell lines and a rat hepatoma cell line, as well as the hAhR with native conformations. We concluded that the newly generated mAbs could be employed in AhR-based bioassays for analysis of environmental contaminants, and held great potential for further revealing the spatial structure of AhR and its biological functions in future studies.

In the forthcoming postgenomic era, identification of regulatory DNA sequences is becoming increasingly important for characterizing DNA-binding proteins and for elucidating the regulatory mechanisms of gene expression. Presently, there lack efficient methods to broadly screen and identify DNA regulatory elements on a large scale. We established herein an efficient strategy to screen regulatory sequences from bacterial artificial chromosome (BAC) DNAs containing human alpha- and beta-globin gene clusters based on polymerase chain reaction and electrophoretic mobility shift assay (EMSA) techniques without purified transcription factors. Twenty-three subclones derived from alpha-BAC DNA by bulk EMSA selection retained the ability to bind nuclear proteins of K562 cells when retested by EMSA. In 19 clones sequenced, 14 are identical to those registered in GenBank and five have one base difference. All of the 24 randomly picked beta-BAC clones showed specific binding with nuclear proteins of K562 cells. In 11 clones sequenced, eight are identical to those registered in GenBank and three have one base difference. This approach could be particularly powerful if combined with other systematic methods for identifying cis-regulatory DNA elements.Key words: gene expression regulation, bacterial artificial chromosome, alpha- and beta-globin gene clusters.

The effects of linoleic acid on hepatopancreatic cell culture of the kuruma prawn, Penaeus vannamei were conducted. The culture system consists of 199 media (M 199) supplemented with 0.060 mol/L NaCl, 1.011g/L glucose, 1000 UI/ml penicillin, 1000 μg/ml treptomycin, 20% heat inactivated fetal calf serum (FCS) for primary cells and 10 % for subculture cells. The content of phosphorus in cultured cells was measured. The results show that the growth condition of cultured hepatopancreas cells in P. vannamei was significantly improved by added 160 μmol/L linoleic acid.

Recently, acetylcholinesterase (AChE, EC 3.1.1.7) has received increased attention in the field of environmental sciences. Evaluation of the effects of environmental contaminants on AChE enzymatic activity not only can reflect, to some extent, the interference with the nervous system, but also can be used for monitoring pollution. Our previous study showed that 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) suppressed neuronal AChE enzymatic activity via transcriptional downregulations mediated by aryl hydrocarbon receptor. In the present study, the effects of several other dioxin-like compounds (DLCs) on neuronal AChE activity were determined, including 1,2,3,7,8-pentachlorodibenzo-p-dioxin, 2,3,7,8-tetrachlorodibenzofuran, 2,3,4,7,8-pentachlorodibenzofuran, and 2,3,7,8-tetrabromodibenzo-p-dioxin. The results showed that the enzymatic activity of AChE was significantly decreased by approximately 15–30 % after exposure to a certain concentrations of the DLCs, whereas incubating neuronal cell lysates directly with these DLCs did not inhibit AChE enzyme. Subsequent molecular mechanism study showed that these chemicals could decrease ACHE promoter activity, as well as AChE T mRNA expression, thereby suggesting the involvements of transcriptional regulation in these effects. These findings on DLCs are similar with those on 2,3,7,8-TCDD, pointing to the possibility that exposure to dioxin and DLCs, which frequently coexist in the contaminated environments, may concurrently interfere with the cholinergic functions via AChE.

Background: Deficits in cognitive functioning have been reported in humans exposed to dioxins and dioxin-like compounds. Evidence suggests that dioxins induce cholinergic dysfunction mediated by hypothyroidism. However, little is known about direct effects of dioxins on the cholinergic system. Objectives: We investigated the action of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on acetylcholinesterase (AChE), a key enzyme in cholinergic neurotransmission. Methods: We used SK-N-SH human-derived neuronal cells to evaluate the effect of dioxin exposure on AChE. Results: We consistently found a significant decrease in enzymatic activity of AChE in cultured neurons treated with TCDD. We also found that, unlike organophosphate pesticides that directly act on the catalytic center of AChE, the suppressive effect of dioxin was through transcriptional regulation. The addition of CH223191, an inhibitor of the aryl hydrocarbon receptor (AhR)-dependent pathway, counteracted the TCDD-induced suppression of AChE, suggesting involvement of the AhR-dependent pathway. The existence of putative dioxin-responsive element (DRE) consensus sequences in the human ACHE promoter region further supported this hypothesis. Consistent with the absence of DRE elements in mouse or rat ACHE promoter regions, suppression of AChE by TCDD did not occur in rat neuronal cells, indicating a potential species-specific effect. Conclusions: In SK-N-SH cells, dioxin suppressed the activity of neuronal AChE via AhR-mediated transcriptional down-regulation. This is the first study to report direct interference by dioxin with the cholinergic neurotransmission system.

Polybrominated diphenyl ethers (PBDEs) as ubiquitous persistent organic pollutants have attracted much attention in recent years. Exposure to PBDEs could induce a high health risk for children. The aim of this study was to investigate the PBDEs exposure of children (9-12 years) from Taizhou, China. Fifty-eight blood samples were collected in one school in a mountainous area in Taizhou. The concentrations of sigma9PBDEs (sum of BDE-28, -47, -99, -100, -153, -154, -183, -197 and -209) ranged from 2.66 to 33.9 ng/g lipid wet (lw) with a median of 7.22 ng/g lw. These concentrations were lower than those of children in USA, but close to European and Asian general population levels. The results showed that children in Taizhou countryside were at a low level of PBDEs exposure. The predominant congener was BDE-209, followed by BDE-28, -47, -197 and -153. High abundance of BDE-209 was consistent with the pollution background of PBDEs in China characterized by high brominated congeners as main pollutants.

The effects of the manganese (Mn) supplemented diets on the level of superoxide anions (O-2) in the hemolymph, and the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) in the muscle of Neocaridina heteropoda were investigated. Manganese sulfate (MnSO4) was added to a basal diet at 0, 20, 40, 60, 80, or 100 μg/g. Diets were fed to triplicate groups of shrimp (0.30±0.11 g, 1.4±0.1 cm) in a recirculating freshwater rearing system for 30 days. The Mn concentration in the rearing water, monitored during feeding, was 1.00±0.02 μg/l. O-2 was lower and antioxidant enzyme activity was higher (p

The effects of dietary Selenium (Se) supplementation on muscle superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) activities and haemolymph superoxide anions ( $$ {\text{O}}_{2}^{ - } $$ ) of Neocaridina heteropoda exposed to ambient nitrite were investigated. The results showed supplementation of Se in diet could enhance the resistance of shrimp to low concentration ambient nitrite. The results demonstrated that Se might have a potentially useful role as an effective antioxidant and resistance to aqueous nitrite in shrimp and the effect of the organic Se was better than that of the inorganic Se.

The effects of a selenium-supplemented diet on the antioxidant enzyme activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) in muscles of the shrimp, Neocaridina heteropoda, were investigated. Purified diets with six levels (0, 0.15, 0.30, 0.45, 0.60, and 0.75 μg/g) of supplemental Se were fed to N. heteropoda for three months. CAT and GPX activity was determined after one month and SOD activity was determined every month. The activity of the enzymes was dose dependant; activity of all three enzymes was significantly higher in shrimp fed Se-sup- plemented diets than in those fed the unsupplemented control diet. SOD activity significantly rose and fell during the three months and was higher in the second month than in the first or third. For all three enzymes, antioxi- dant activity reached a maximum when the Se concentration was 0.45 μg/g.

To immobilize DNA fragments onto magnetic beads coated with streptavidin for isolation purpose, it is important to label one biotin molecule at one terminus of DNA fragment. After failure to label long DNA with biotin by PCR and filling-in reaction, a 9.2 kb DNA was labeled with biotin by a modified ligation strategy. A simple method is also reported to detect the quantity and integrity of DNA immobilized on the magnetic beads.