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This article is devoted to the optimal protocol for the leader-following consensus of second-order multiagent systems. Remarkably, the global consensus cost functional and the directed topology are pregiven, and the optimal protocol to be sought is distributed. This makes the Riccati-based strategies inapplicable, by which merely centralized protocol can be derived. As the main contribution of this article, an effective strategy of seeking a distributed optimal protocol is proposed for second-order agents over the digraph of the directed tree. Detailedly, the feasibility of distributed optimal protocol is first affirmed, that is, the existence of optimal gain parameters can be guaranteed. Then, by recursively deriving the completely explicit formulas of the consensus errors of relative position and velocity, an online implementable algorithm is developed to achieve the parameterization of the cost functional, that is, to obtain the explicit formula of the cost functional with respect to gain parameters of all agents. Lastly, the desired optimal gain parameters are obtained by minimizing the explicit formula. [ABSTRACT FROM AUTHOR]

In this article, a distributed energy management strategy is proposed for smart grid with stochastic wind power. The different Weibull probability distribution function (PDF) of wind power during different operation intervals, coupled with ramp rate limits of thermal generators across operation intervals, is considered in this operation cost optimization problem. Under multiagent system communication framework, we first decompose the problem into subproblems associated to operation interval. For each operation interval, parameters of Weibull PDF are estimated by maximum likelihood method according to wind speed obtained by wind speed forecast model of committed wind turbine. Then, a consensus-based alternating direction method of multipliers (ADMM) is proposed to get the optimal operation plan for all committed generators, where Armijo line search algorithm is employed to adaptively obtain the step size in the iterations. The simulation results show that the proposed consensus-based ADMM outperforms distributed projected gradient method in previous study on energy management with wind power; the proposed distributed strategy is valid for short-term energy management for smart grid with stochastic wind power. [ABSTRACT FROM AUTHOR]

This paper considers the global stabilization for a class of uncertain nonlinear systems with unknown powers, unknown control directions, and unknown nonlinearities. Mainly due to the presence of the unknown powers which have not known upper bound, no existing methods are applicable to the control problem to be solved. In this paper, to compensate the serious system uncertainties and particularly to overcome the major obstruction from unknown powers, we appeal to the mechanism of switching adaptive feedback. By flexibly combining the domination and the method of adding a power integrator, we propose a new adaptive controller design, whose design parameters are tuned online based on a switching logic. The designed controller will become operative as long as finite switchings happen and will not lead to Zeno phenomenon, and can guarantee the global boundedness as well as ultimate convergence of the resulting closed-loop system. Two numerical examples are given to demonstrate the effectiveness of the developed design scheme. [ABSTRACT FROM AUTHOR]

In the near future, plug-in electric vehicles (PEVs) will dominate the car market. The peak-valley difference would increase greatly due to the random nature of PEVs charging behaviors. In this paper, a new problem on studying the dynamic economic/emission dispatch (DEED) including PEVs for peak shaving and valley filling is proposed, and furthermore, the effect caused by different vehicle-to-grid (V2G) and grid-to-vehicle (G2V) loads on DEED is analyzed. The optimization model of the problem is constructed including several practical constraints, such as power flow constraints and ramp rate limits. The battery degradation cost is also included, which reshapes the objective function of DEED. Based on the model, a strategy for DEED including PEVs for peak shaving and valley filling is given, and a multiobjective optimization algorithm is adopted to solve the proposed problem. To demonstrate the feasibility and effectiveness of the proposed strategy, three DEED cases are considered under different V2G power. The analysis of the effect on fuel cost and emission caused by different V2G power shows that the proposed strategy can effectively reduce the emission and cut down the investment in peak load plants. [ABSTRACT FROM AUTHOR]

We present a hybrid metaheuristic optimization algorithm for solving economic dispatch problems in power systems. The proposed algorithm, based on bat algorithm, combines chaotic map and random black hole model together. Chaotic map is used to prevent premature convergence, and the random black hole model is helpful not only in avoiding premature convergence, but also in increasing the global search ability, enlarging exploitation area and accelerating convergence speed. The pseudocode and related parameters of the proposed algorithm are also given in this paper. Different from other related works, the costs of conventional thermal generators and random wind power are both included in the cost function because of the increasing penetration of wind power. The proposed algorithm has no requirement on the convexity or continuous differentiability of the cost function, although the effect on fuel cost, caused by the underestimation and overestimation of wind power, is included. This makes it feasible to take more practical nonlinear constraints into account, such as prohibited operating zones and ramp rate limits. Three test cases are given to illustrate the effectiveness of the proposed method. [ABSTRACT FROM AUTHOR]

This paper is concerned with event-triggered bounded consensus tracking for a class of second-order nonlinear multi-agent systems with uncertainties (MASs). Remarkably, the considered MASs allow multiple uncertainties, including unknown control coefficients, parameterized unknown nonlinearities, uncertain external disturbances, and the leader's control input being unknown. In this context, a new estimate-based adaptive control protocol with a triggering mechanism is proposed. We rule out Zeno behavior by testifying that the lower bound on the interval between two consecutive events is positive. It is shown that under the designed protocol, all signals caused by the closed-loop systems are bounded globally uniformly and tracking errors ultimately converge to a bounded set. The effectiveness of the devised control protocol is demonstrated through a simulation example. [ABSTRACT FROM AUTHOR]

This paper is devoted to the semiglobal stabilization via output-feedback for a class of uncertain nonlinear systems. Remark that the systems in question contain an unknown control coefficient which inherently depends on the system output and allow larger-than-two order growing unmeasurable states which is the obstruction of global stabilization via output-feedback. By introducing a recursive reduced-order observer and combining with saturated state estimate, a desired output-feedback controller is explicitly constructed for the systems. Under the appropriate choice of design parameters, the controller can make the closed-loop system semiglobally attractive and locally exponentially stable at the origin. A simulation example is provided to illustrate the effectiveness of the proposed approach. [ABSTRACT FROM AUTHOR]

This study considers the global adaptive control design for a class of high‐order uncertain non‐linear systems. Different from the existing results, the systems under investigation have serious unknowns which cannot be bounded by any known constants, and particularly have double control input channels, that is, the scalar control input directly affects two one‐dimensional subsystems. Inspired by the author's recent results, by skillfully combing the method of adding a power integrator and some adaptive techniques, an adaptive controller is successfully constructed which can guarantee the asymptotical convergence of the system states for any given initial conditions. A simulation example is given to demonstrate the validity of the obtained theoretical results. [ABSTRACT FROM AUTHOR]

This paper researches the fixed-time leader-following consensus problem for nonlinear multi-agent systems (MASs) affected by unknown disturbances under the jointly connected graph. In order to achieve control goal, this paper designs a fixed-time consensus protocol, which can offset the unknown disturbances and the nonlinear item under the jointly connected graph, simultaneously. In this paper, the states of multiple followers can converge to the state of the leader within a fixed time regardless of the initial conditions rather than just converging to a small neighborhood near the leader state. Finally, a simulation example is given to illustrate the theoretical result. [ABSTRACT FROM AUTHOR]

Benzene is a recognized environmental leukemogen, however, the mechanisms for its carcinogenesis have not been fully elucidated. Recently, miR-221, a suggested oncogene involved in a number of malignancies, has been detected with elevated expression levels in blood cells of patients with leukemia. To explore whether benzene exposure has an effect on the expression of miR-221, a population based cross-sectional study was conducted in southern China, with 97 petrol station attendants as the exposure group and 103 general residents as the control group. Plasma benzene was analyzed by using GC∖MS. miR-221 in peripheral blood lymphocytes were measured by qRT-PCR and the ΔCt value for each sample was calculated by normalizing the Ct value for miR-221 with U6 RNA (i.e., ΔCt = Ct miR-221 − Ct U6 ). Potential confounding factors were taken into account. Pearson correlation, univariate and multivariate logistic regression were performed in statistical analysis. The results showed that the air concentrations of benzene were significantly higher in petrol stations than in control sites ( P < 0.05); The levels of benzene and miR-221 in exposure group were both significantly higher than in control group ( P < 0.05) and there was a significant positive correlation between the two indexes ( r = 0.851, P < 0.05); An association between benzene levels and the ΔCt values for miR-221 was identified by univariate and multivariate logistic analysis (OR 0.274; 95%CI 0.117, 0.396). Our investigation indicates that benzene exposure may be related to elevated miR-221 expression in human lymphocytes. [ABSTRACT FROM AUTHOR]

Tris(2-butoxyethyl) phosphate (TBOEP) is an organophosphorus flame retardant ubiquitously present in the environment and even the human body. TBOEP is toxic in multiple tissues, which forms dealkylated and hydroxylated metabolites under incubation with human hepatic microsomes; however, the impact of TBOEP metabolism on its toxicity, particularly mutagenicity (typically requiring metabolic activation), is left unidentified. In this study, the mutagenicity of TBOEP in human hepatoma cell lines (HepG2 and C3A) and the role of specific CYPs were studied. Through molecular docking, TBOEP bound to human CYP1A1, 1B1, 2B6 and 3A4 with energies and conformations favorable for catalyzing reactions, while the conformations of its binding with human CYP1A2 and 2E1 appeared unfavorable. In C3A cells (endogenous CYPs being substantial), TBOEP exposing for 72 h (2-cell cycle) at low micromolar levels induced micronucleus, which was abolished by 1-aminobenzotriazole (inhibitor of CYPs); in HepG2 cells (CYPs being insufficient) TBOEP did not induce micronucleus, whose effect was however potentiated by pretreating the cells with PCB126 (CYP1A1 inducer) or rifampicin (CYP3A4 inducer). TBOEP induced micronucleus in Chinese hamster V79-derived cell lines genetically engineered for stably expressing human CYP1A1 and 3A4, but not in cells expressing the other CYPs. In C3A cells, TBOEP selectively induced centromere protein B-free micronucleus (visualized by immunofluorescence) and PIG-A gene mutations, and elevated γ-H2AX rather than p-H3 (by Western blot) which indicated specific double-strand DNA breaks. Therefore, this study suggests that TBOEP may induce DNA/chromosome breaks and gene mutations in human cells, which requires metabolic activation by CYPs, primarily CYP1A1 and 3A4. [Display omitted] • Tris(2-butoxyethyl) phosphate (TBOEP) induced DNA breaks and gene mutations. • TBOEP formed micronuclei in human hepatoma C3A cells by a clastogenic mechanism. • Mutagenicity of TBOEP was dependent on metabolic activation by human CYP1A1 and 3A4. • Pretreating HepG2 cells with AhR and PXR activators potentiated the effect of TBOEP. [ABSTRACT FROM AUTHOR]

Aflatoxin B1 (AFB1) is the most toxic mycotoxin and a proven human carcinogen that requires metabolic activation, known by cytochrome P450 (CYP) 1A2 and 3A4. Previous evidence showed that AFB1 is activated by human recombinant CYP1A1 expressed in budding yeast. Yet, the toxicity, in particular the genotoxicity of the reactive metabolites formed from AFB1 remains unclear. Humans could be exposed to both AFB1 and benzo(a)pyrene (BaP) simultaneously, thus we were interested in their combined genotoxic effects subsequent to metabolic activation by CYP1A1. In this study, molecular docking of AFB1 to human CYP1A1 indicated that AFB1 is valid as a substrate. In the incubations with AFB1 in human CYP1A1-expressed microsomes, AFM1 as a marking metabolite of AFB1 was detected. Moreover, AFB1 induced micronucleus formation in a Chinese hamster V79-derived cell line and in a human lung epithelial BEAS-2B cell line, both expressing recombinant human CYP1A1, V79-hCYP1A1 and 2B-hCYP1A1 cells, respectively. Immunofluorescence of centromere protein B stained micronuclei was dominant in AFB1-treated BEAS-2B cells exposed to AFB1, suggesting an aneugenic effect. Moreover, AFB1 elevated the levels of ROS, 8-OHdG, AFB1-DNA adduct, and DNA breaks in 2B-hCYP1A1 cells, compared with those in the parental BEAS-2B cells. Meanwhile, AFB1 increased CYP1A1, RAD51, and γ-H2AX protein levels in 2B-hCYP1A1 cells, which were attenuated by the CYP1A1 inhibitor bergamottin. Co-exposure of AFB1 with BaP increased 8-OHdG, RAD51, and γ-H2AX levels (indicating DNA damage). In conclusion, AFB1 could be activated by human CYP1A1 for potent aneugenicity, which may be further enhanced by co-exposure to BaP. • AFB1 could be activated by human CYP1A1 for potent aneugenicity. • AFM1 is formed by AFB1 incubated in human CYP1A1-expressed microsomes. • AFB1 and BaP coexposure enhanced the genotoxic effects associated with human CYP1A1 activity. [ABSTRACT FROM AUTHOR]

The land surface temperature (LST) changes in North America are very abnormal recently, but few studies have systematically researched these anomalies from several aspects, especially the influencing forces. After reconstructing higher quality MODIS monthly LST data (0.05° * 0.05°) in 2002–2018, we analyzed the LST changes especially anomalous changes and their driving forces in North America. Here we show that North America warmed at the rate of 0.02 °C/y. The LST changes in three regions, including frigid region in the northwestern (0.12 °C/y), the west coast from 20°N–40°N (0.07 °C/y), and the tropics south of 20°N (0.04 °C/y), were extremely abnormal. The El Nino and La Nina were the main drivers for the periodical highest and lowest LST, respectively. The North Atlantic Oscillation was closed related to the opposite change of LST in the northeastern North America and the southeastern United States, and the warming trend of the Florida peninsula in winter was closely related to enhancement of the North Atlantic Oscillation index. The Pacific Decadal Oscillation index showed a positive correlation with the LST in most Alaska. Vegetation and atmospheric water vapor also had a profound influence on the LST changes, but it had obvious difference in latitude. [ABSTRACT FROM AUTHOR]

Background: Postpartum depression (PPD) is prevalent and may present major adverse impacts on mother and child health. According to previous studies, mostly from the western society, PPD may have complicated etiologies, such as genetic, social and psychological factors. The aim of this study was to explore the associations of some social and clinical factors, particularly those unique in Chinese, with significant PPD symptoms.Methods: A sample of 556 pregnant women in their 36th to 40th gestational week were randomly recruited in a cross-sectional study using a self-reported questionnaire, which collected maternal sociodemographic and clinical information. During their 2nd to 4th postpartum months, 522 participants responded to our screening of significant PPD symptoms, based on a score of Edinburgh Postnatal Depression Scale ≥9.Results: A total of 90 (17.3%) participants were identified with significant PPD symptoms, and the following factors were observed more frequently in women with significant PPD symptoms (PPD+) than with fewer symptoms (PPD-): intensive involvement of parents-in-law in a participant's life (living together with her, taking care of her, or discriminating against a female baby), lack of support from husband, cesarean delivery, and breast milk insufficiency (supplemented with formula). After multiple logistic regression analysis, parents-in-law's preference to baby boy while devaluing baby girl, dissatisfaction with husband's support, cesarean delivery, and mixed feeding were strongly associated with significant PPD symptoms.Conclusion: The potential risk factors for significant PPD symptoms, i.e., "son preference" custom, cesarean delivery and mixed feeding, deserve confirmation in continued, especially clinical diagnosis-based longitudinal studies. [ABSTRACT FROM AUTHOR]

Heavy metals, such as cadmium and lead, are ubiquitously present as single substances and compounds in the environment. These substances have various and overlapping health effects. Consumption of contaminated foods is the main pathway of the human exposure, however, estimation of their dietary exposure in combination with health risk analysis, particularly at various endpoints, has rarely been reported. In this study, we integrated relative potency factor (RPF) analysis into the margin of exposure (MOE) model to evaluate the health risk of combined heavy metal (including cadmium, arsenic, lead, chromium, and nickel) exposure in the residents in Guangzhou, China, after quantifying the heavy metals in various food samples and estimating their dietary exposure. The results indicated that rice, rice products and leafy vegetables contributed primarily to the dietary exposure of all metals except arsenic, which exposed the population largely through consumption of sea-foods. With all the five metals contributing to nephro- and neurotoxicity, the 95% confidence limits of MOE for the residents were clearly below 1.0 in the 3∼6-year group, suggesting a recognizable risk to young children. This study provides substantial evidence for the non-negligible health risk in young children due to increased heavy metal exposure,at least on some toxicity targets. [Display omitted] • Relative potency factor and margin of exposure were used for risk analysis of metals. • Rice/rice products/leafy vegetables contributed largely to Cd, Pb, Cr & Ni exposure. • Multiple toxicity endpoints were evaluated based on combined metal exposure. • Children at 3–6 years were especially prone to dietary metal-associated health risks. [ABSTRACT FROM AUTHOR]

Abstract Polychlorinated biphenyls (PCBs) as a group of persistent organic pollutants are confirmed human carcinogens; however, their mutagenicity remains mostly unknown. We have reported the mutagenicity of some PCBs with one to four chlorines in mammalian cells expressing human CYP2E1. To further explore the structural requirements for the mutagenicity of PCBs, eight tri- and tetrachlorobiphenyls untested before were investigated for the induction of gene mutations and micronuclei in a V79-derived cell line expressing both human CYP2E1 and sulfotransferase (SULT) 1A1 (V79-hCYP2E1-hSULT1A1), with SULT1A1 activity inhibited by pentachlorophenol, a potent SULT1 inhibitor. 2,2′,6-Tri-, 2,3′,6-tri, 2,4′,6-tri-, and 2,2′,5-trichlorobiphenyls (PCBs 19, 27, 32, and 18, respectively) induced micronuclei and gene mutations in V79-hCYP2E1-hSULT1A1 cells, at potencies slightly higher than 2,6-dichlorobiphenyl, but one order of magnitude below that by 2,3,3′- and 2,3,4′-trichlorobiphenyls as reported recently; in the parental V79-Mz cells, they were nonmutagenic and weak in micronuclei induction. Among the four tetrachlorobiphenyls with varying number of ortho chlorines, 2,3,3′,4′-tetrachlorobiphenyl (PCB 56) induced both micronuclei and gene mutations in V79-hCYP2E1-hSULT1A1 cells with a potency greater than the above compounds; however, 2,2′,3,3′-tetrachlorobiphenyl was equivocal and 2,2′,3,6′-tetra- and 2,2′,6,6′-tetrachlorobiphenyls inactive in V79-hCYP2E1-hSULT1A1 cells. Immunofluorescent staining of micronuclei formed by PCBs 32 and 56 in V79-hCYP2E1-hSULT1A1 cells with centromere protein B antibodies indicated that they were predominantly whole chromosomes, implying aneugenic potentials. This study suggests that tri- and tetrachlorobiphenyls with a single ortho chlorine can be most mutagenic under activation by human CYP2E1, and greater numbers of ortho chlorines may cause a drastic decline in the activity, especially for tetrachlorobiphenyls. Highlights • Activation of tetra-Cl-PCBs by CYP2E1 is limited by the increase in ortho chlorines. • Distinct structure-mutagenicity relationships exist between tri- and tetra-Cl-PCBs. • Human CYP2E1 can activate some noncoplanar PCBs for aneugenic potentials. [ABSTRACT FROM AUTHOR]

As a new-type flame retardant and toxic substance, triphenyl phosphate (TPP) is a ubiquitous pollutant present even in human blood. TPP is transformed by human CYP enzymes to oxidized/dealkylated metabolites. The impact of TPP metabolism on its toxicity, however, remains unclear. In this study, the genotoxicity of TPP in several mammalian cell lines and its relevance to CYP/sulfortransferase (SULT) activities were investigated. The results indicated that TPP induced micronucleus formation at ≥1 μM concentrations in a human hepatoma (C3A, endogenous CYPs being substantial) cell line, which was abolished by 1-aminobenzotriazole (CYPs inhibitor). In cell line HepG2 (parental to C3A with lower CYP expression) TPP was inactive up to 10 μM, while pretreatment with ethanol (CYP2E1 inducer), PCB 126 (CYP1A inducer), or rifampicin (CYP3A inducer) led to micronucleus formation by TPP. In V79-Mz and V79-derived cells expressing human CYP1A1 TPP was inactive (up to 32 μM), and in cells expressing human CYP1B1, 2B6 and 3A4 it induced micronucleus weakly (positive only at 32 μM). However, TPP induced micronucleus potently in V79-derived cells expressing human CYP1A2, while this effect was drastically reduced by human SULT1A1 co-expression; likewise, TPP was inactive in cells expressing both human CYP2E1 and SULT1A1, but became positive with pentachlorophenol (inhibitor of SULT1) co-exposure. Moreover, in C3A cells TPP selectively induced centromere-free micronucleus (immunofluorescent assay), and TPP increased γ-H2AX (by Western blot, indicating double-strand DNA breaks). In conclusion, this study suggests that TPP is potently clastogenic, human CYP1A2 and 2E1 being major activating enzymes while SULT1A1 involved in detoxification. • Triphenyl phosphate (TPP) induced genotoxic effect in mammalian cells. • The genotoxicity of TPP depended on metabolic activation by human CYP enzymes. • Human CYP1A2 and 2E1 were the major metabolic enzymes involved in activating TPP. • The mode of TPP-induced chromosome damage appeared to be purely clastogenesis. [ABSTRACT FROM AUTHOR]

Polychlorinated biphenyls (PCBs) are a group of persistent organic pollutants with confirmed carcinogenicity to humans. Metabolic activation of lower chlorinated PCBs to genotoxic metabolites may involve hydroxylation and further oxidation, and some hydroxylated metabolites may be sulfo-conjugated. However, the genotoxicity of individual PCB compounds is largely unknown. In this study, 15 mono- and dichlorobiphenyls were investigated for genotoxicity using the micronucleus and Hprt mutagenicity assays in a Chinese hamster V79-derived cell line expressing both human cytochrome P450 (CYP) 2E1 and human sulfotransferase (SULT) 1A1 (V79-hCYP2E1-hSULT1A1). All tested compounds were inactive in both assays in V79 control cells. However, eight dichlorobiphenyls strongly induced micronuclei and other congeners were weakly positive for this endpoint in V79-hCYP2E1-hSULT1A1 cells. The effects of each PCB in V79-hCYP2E1-hSULT1A1 cells were abolished or reduced in the presence of a CYP2E1 inhibitor (1-aminobenzotriazole), or enhanced by pretreatment of the cells with (CYP2E1-inducing) ethanol, while the genotoxicity was not significantly affected by a SULT1 inhibitor (pentachlorophenol). As representative dichlorobiphenyls, PCB 5, 10, 8 and 11 (2,3-, 2,5-, 2,4ʹ- and 3,3ʹ-dichlorobiphenyl, respectively) strongly induced Hprt gene mutations in V79-hCYP2E1-hSULT1A1 cells in a concentration-dependent manner. This is the first indication that human CYP2E1 is capable of converting a series of dichlorobiphenyls to strong mutagens. [ABSTRACT FROM AUTHOR]

ObjectiveTo evaluate the relationship between dietary habits, physical activity and cognitive views and the risk of gestational diabetes mellitus (GDM) in Chinese women.DesignA cross-sectional study to explore the potential risk factors of GMD through the International Physical Activity Questionnaire, an FFQ and a self-designed structured questionnaire, respectively.SettingGuangzhou, Guangdong Province, China.SubjectsChinese pregnant women (n 571) who underwent a 75-g oral glucose tolerance test at their 24th to 28th gestational week.ResultsThirteen per cent of the investigated women were identified as having GDM, and an increased intake of local featured foods and lower physical activity were observed in the GDM-positive group v. the GDM-negative group. Women who regarded early-pregnancy morning sickness as relevant to fetal abnormalities and those with unlimited dietary intake after the ending of morning sickness both had an increased risk for GDM (P = 0·018 and P = 0·038, respectively). After multiple logistic regression analysis, cognitive views for unlimited food intake subsequent to morning sickness, increased consumption of energy-dense snack foods and high-glycaemic-index fruits were strongly associated with the risk of GDM (OR = 1·911, P = 0·032; OR = 1·050, P = 0·001; and OR = 1·002, P = 0·017, respectively).ConclusionsLocal featured foods and incorrect cognitive views on pregnancy-related health were closely related to the risk of GDM in Chinese women. Intensive health education about pregnancy physiology and reasonable dietary and physical exercise behaviours should be strengthened for the control of GDM. [ABSTRACT FROM AUTHOR]

Polybrominated biphenyl ethers (PBDEs) are a group of persistent organic pollutants with endocrine-disrupting, neurotoxic, tumorigenic and DNA-damaging activities. They are hydroxylated by human liver microsomal CYP enzymes, however, their mutagenicity remains unknown. In this study, 2,2′,4,4′-tetrabromobiphenyl ether (BDE-47, relatively abundant in human tissues) was investigated for micronuclei induction and DNA damage in mammalian cells. The results indicated that BDE-47 up to 80 μM under a 6 h/18 h (exposure/recovery, covering 2 cell cycles) regime did not induce micronuclei in V79-Mz and V79-derived cell lines expressing human CYP1A1 or 1A2, while it was moderately positive in human CYP2B6-, 2E1-and 3A4-expressing cell lines (V79-hCYP2B6, V79-hCYP2E1-hSULT1A1 and V79-hCYP3A4-hOR, respectively). Following 24 h exposure, BDE-47 induced micronuclei in V79-hCYP2E1-hSULT1A1 and V79-hCYP3A4 cells at increased potencies. In the human hepatoma (HepG2) cells BDE-47 (48 h exposure) was inactive up to 40 μM, however, pretreatment of the cells with ethanol (0.2%, v:v, inducer of CYP2E1) or rifampicin (10 μM, inducer of CYP3A4) led to significant micronuclei formation by BDE-47; pretreatment with bisphenol AF (100 nM) also potentiated BDE-47-induced micronuclei formation (which was blocked by a CYP2E1 inhibitor trans -1,2-dichloroethylene or a CYP3A inhibitor (ketoconazole). Immunofluorescent staining of centromere protein B with the micronuclei formed by BDE-47 in HepG2 cells pretreated with ethanol or rifampicin demonstrated selective formation of centromere-containing micronuclei. The increased phosphorylation of both histones H2AX and H3 in HepG2 by BDE-47 also indicated an aneugenic potential. Therefore, this study suggests that BDE-47 is an aneugen activated by several human CYP enzymes. [Display omitted] • 2,2′,4,4′-Tetrabromobiphenyl ether (BDE-47) is aneugenic in mammalian cells. • The aneugenicity of BDE-47 depends on metabolic activation by human CYP enzymes. • Human CYP3A4 and 2E1 might be the major enzymes activating BDE-47. [ABSTRACT FROM AUTHOR]

1-Methylpyrene (1-MP) is a ubiquitous environmental pollutant and rodent carcinogen. Its mutagenic activity depends on sequential activation by various CYP and sulfotransferase (SULT) enzymes. Previously we have observed induction of micronuclei and mitotic arrest by 1-MP in a Chinese hamster (V79)-derived cell line expressing both human CYP1A2 and SULT1A1 (V79-hCYP1A2-hSULT1A1), however, the mode of chromosome damage and the involvement of mitotic tubulin structures have not been clarified. In this study, we used immunofluorescent staining of centromere protein B (CENP-B) with the formed micronuclei, and that of β- and γ-tubulin reflecting the structures of mitotic spindle and centrioles, respectively, in V79-hCYP1A2-hSULT1A1 cells. The results indicated that 1-MP induced micronuclei in V79-hCYP1A2-hSULT1A1 cells from 0.125 to 2 μM under a 24 h/0 h (exposure/recovery) regime, while in the parental V79-Mz cells micronuclei were induced by 1-MP only at concentrations ≥ 8 μM; in both cases, the micronuclei induced by 1-MP were predominantly CENP-B positive. Following 54 h of exposure, 1-MP induced mitotic spindle non-congression and centrosome amplification (multipolar mitosis) in V79-hCYP1A2-hSULT1A1 cells, and anaphase/telophase retardation, at concentrations ≥ 0.125 μM with concentration-dependence; while in V79-Mz cells it was inactive up to 8 μM. This study suggests that in mammalian cells proficient in activating enzymes 1-MP may induce chromosome loss and mitotic disturbance, probably by interfering with the mitotic spindle and centrioles. 1-Methylpyrene is potently aneugenic in metabolism-proficient mammalian cells. 1-Methylpyrene may disrupt mitotic apparatus by interfering with tubulin. 1-Methylpyrene may retard mitotic progression. [ABSTRACT FROM AUTHOR]

• Subchronic arsenic exposure via food changes the gut microbiome. • Feces might be the main excreting pathway for arsenic from food exposure. • The toxicity of arsenic in staples should be comprehensively evaluated. • Gut microbiome interaction might be disturbed by arsenic. • Arsenic exposure would disturb carbohydrates, lipid, and amino acids metabolism of gut bacteria. Arsenic, a global pollutant and a threshold-free primary carcinogen, can accumulate in rice. Previous studies have focused on arsenic poisoning in drinking water and the effects on gut microbes. The research on arseniasis through food, which involves the bio-transformation of arsenic, and the related changes in gut microbiome is insufficient. Mice were exposed from animal feed prepared with four arsenic species (iAsIII, iAsV, MMA, and DMA) at a dose of 30 mg/kg according to the arsenic species proportion in rice for 30 days and 60 days. The levels of total arsenic (tAs) and arsenic species in mice feces and urine samples were determined using ICP-MS and HPLC-ICP-MS, respectively. 16S rRNA and ITS gene sequencing were conducted on microbial DNA extracted from the feces samples. At 30 days and 60 days exposure, the tAs levels excreted from urine were 0.0092 and 0.0093 mg/day, and tAs levels in feces were 0.0441 and 0.0409 mg/day, respectively. We found significant differences in arsenic species distribution in urine and feces (p < 0.05). In urine, the predominant arsenic species were iAsIII (23% and 14%, respectively), DMA (55% and 70%, respectively), and uAs (unknown arsenic, 14% and 10%, respectively). In feces, the proportion of major arsenic species (iAsV, 26% and 21%; iAsIII, 16% and 15%; MMA, 14% and 14%; DMA, 19% and 19%; and uAs, 22% and 29%, respectively) were evenly distributed. Microbiological analysis (MRPP test, α- and β-diversities) showed that diversity of gut bacteria was significantly related to arsenic exposure through food, but diversity of gut fungi is less affected. Manhattan plot and LEfSe analysis showed that arsenic exposure significantly changes microbial taxa, which might be directly associated with arsenic metabolism and diseases mediated by arsenic exposure, such as Deltaproteobacteria , Polynucleobacter , Saccharomyces , Candida , Amanitaceae, and Fusarium. Network analysis was used to identify the changing hub taxa in feces along with arsenic exposure. Function predicting analysis indicated that arsenic exposure might also significantly increase differential metabolic pathways and would disturb carbohydrates, lipid, and amino acids metabolism of gut bacteria. The results demonstrate that subchronic arsenic exposure via food significantly changes the gut microbiome, and the toxicity of arsenic in food, especially in staples, should be comprehensively evaluated in terms of the disturbance of microbiome, and feces might be the main pathway through which arsenic from food exposure is excreted and bio-transformed, providing a new insight into the investigation of bio-detoxification for arseniasis. [ABSTRACT FROM AUTHOR]