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The appinite–granite association has been found in various tectonic regimes related to recent subduction, arc-continent or continent–continent collision and post-collision (orogen), and appinites generally originate from recently subduction-modified lithospheric mantle. We conducted a study on a rarely reported appinite–granite association formed in an intracontinental regime, the Zhangjiafang–Qinglongshan complex (ZQC), in which the appinites were derived from an ancient sub-continental lithospheric mantle (SCLM). The ZQC is located in the western Wugongshan domain, and consists of basaltic to intermediate appinites and granitoids. Ten dated samples (including massive and gneissoid granitoids, hornblende gabbro, and diorite) give zircon 206 Pb/ 238 U ages ranging from 444 ± 3 Ma to 452 ± 4 Ma, indicating that these various lithologies were emplaced synchronously. The basaltic appinites show radiogenic 87 Sr/ 86 Sr i (0.71016–0.71431) and negative ε Nd (t) (− 6.1 to − 8.9) and zircon ε Hf (t) (− 4.2 to − 7.5) values. Combined with regional geological background, an origin from the Neoproterozoic metasomatised SCLM can be inferred for the appinites in the Wugongshan domain. The granitoids are peraluminous and almost high-K calc–alkaline to shoshonitic. They exhibit a wide range of isotopic compositions ( 87 Sr/ 86 Sr i = 0.70828–0.71857, ε Nd (t) = − 6.2 to − 10.5, zircon ε Hf (t) = − 9.5 to − 26.6). Some of the granitoids display the most evolved Sr–Nd isotopic signatures among all the studied lithologies, which are consistent with those of the middle to upper crust, suggesting a pure crustal origin. Other granitoids show relatively mafic composition and less evolved isotopic signature. The intermediate appinites have intermediate chemical compositions between those of the basaltic appinites and granitoids, and similar Sr–Nd isotopic compositions to those of the basaltic appinites that have relatively evolved composition and isotopic signature. The petrographical and the geochemical studies, as well as magma mixing and mingling between mafic magma and felsic magma observed in field work, indicate that the ZQC was formed by several complex magmatic processes including assimilation and fractional crystallization (AFC) of a basaltic magma derived from an enriched mantle, magma mixing and mingling, fractional crystallization of a crust-derived felsic magma. The contribution of the Neopreoterozoic subduction-modified lithospheric mantle to the early Paleozoic granitoids in South China has been poorly constrained due to its evolved isotopic signatures (such as negative ε Nd (t) and ε Hf (t) values, high initial ratio of 87 Sr/ 86 Sr) and few studies on the early Paleozoic basaltic–felsic rock association. Our work here suggests that the Wugongshan appinite–granite association was formed in an intracontinental orogen, and the ancient enriched mantle may have had a significant chemical contribution to the formation of some of the Paleozoic peraluminous granites in South China. [ABSTRACT FROM AUTHOR]

Abstract: Palaeozoic mafic igneous rocks are potentially significant in constraining the tectonic nature and evolution of the Kwangsian Orogeny in the eastern South China Block, yet they have received little attention because of their limited outcrop. Geochemistry and geochronology was carried out on newly identified Ordovician ultramafic–mafic appinites in the Wugongshan Domain of the Cathaysia Block. Seven appinite samples yielded 206Pb/238U crystallisation ages ranging from 452±4Ma to 473±3Ma. Abundant 480–500Ma zircon xenocrysts and/or inherited zircons were found in the appinites, possibly indicating an earlier magmatism episode in the early Palaeozoic period. The Wugongshan appinites are ultramafic to mafic in composition, and the ultramafic rocks display features of cumulates (high concentrations of MgO, Fe2O3t, Cr, Ni, and low concentrations of total alkali and total rare earth elements [REE]). The appinite geochemistry displays: relatively flat chondrite normalised REE patterns with slight enrichment in light REE and weak negative Eu anomalies; enrichment in large-ion lithophile elements (such as Rb, K), and weak depletion in Nb–Ta in primitive mantle normalised trace element patterns. We suggest that the Wugongshan appinites likely originated from an ancient metasomatised mantle, and that crustal assimilation, fractional crystallisation (AFC), magma mingling and hydration were involved in the petrogenetic process, based on the combination of geochemistry, crust-like bulk Sr, Nd and zircon Hf isotopic compositions (εNd (t)=−8.2 to −3.2, initial 87Sr/86Sr ratios of 0.7067–0.7144, zircon εHf (t) values peaking at −9 to −3) and regional geological data. Further considering the alignment and chronology of the appinites, we suggest that the appinitic magmas probably were emplaced along the Jiangshan–Shaoxing Fault in a local extensional zone in an intracontinental regime in the early Palaeozoic. [Copyright &y& Elsevier]

Highlights: [•] Fengdingshan granites and Taoyuan Complex were formed in Silurian period. [•] Fengdingshan granites were formed by reworking of Neoproterozoic basaltic crust. [•] Taoyuan mafic rocks originated from a previously metasomatized lithospheric mantle. [•] The Fengdingshan and Taoyuan Plutons were formed in a post-orogenic collapse stage. [•] Nd–Hf decoupling may be a fingerprint of an ancient oceanic subduction. [ABSTRACT FROM AUTHOR]

• Causal interactions between the CEN and DMN in depressed patients were investigated by spectral dynamic causal modeling. • Inhibitory influences from the CEN to the DMN were detected with node-level PEB analyses. • Patients with MDD showed increased effective connectivity within the CEN. • Decreased connectivity from regions of the CEN to DMN was found in the patients. Two different but interacting neural systems exist in the human brain: the task positive networks and task negative networks. One of the most important task positive networks is the central executive network (CEN), while the task negative network generally refers to the default mode network (DMN), which usually demonstrates task-induced deactivation. Although previous studies have clearly shown the association of both the CEN and DMN with major depressive disorder (MDD), how the causal interactions between these two networks change in depressed patients remains unclear. In the current study, 99 subjects (43 patients with MDD and 56 healthy controls) were recruited with their resting-state fMRI data collected. After data preprocessing, spectral dynamic causal modeling (spDCM) was used to investigate the causal interactions within and between the DMN and CEN. Group commonalities and differences in causal interaction patterns within and between the CEN and DMN in patients and controls were assessed by a parametric empirical Bayes (PEB) model. Both subject groups demonstrated significant effective connectivity between regions of the CEN and DMN. In particular, we detected inhibitory influences from the CEN to the DMN with node-level PEB analyses, which may help to explain the anticorrelations between these two networks consistently reported in previous studies. Compared with healthy controls, patients with MDD showed increased effective connectivity within the CEN and decreased connectivity from regions of the CEN to DMN, suggesting impaired control of the DMN by the CEN in these patients. These findings might provide new insights into the neural substrates of MDD. [ABSTRACT FROM AUTHOR]

Background: To determine the predictive values of sperm parameters pre- and post-processing by density gradient centrifugation for clinical pregnancy rates (CPRs) following artificial insemination by husband (AIH) in infertile Chinese couples.Methods: A total of 3,522 AIH cycles from 1,918 couples were retrospectively analyzed. The parameters were compared between the pregnant and non-pregnant groups and further between different etiological groups (Male-factor, Both-male-and-female-factor, and Other-factor). Multivariate logistic regression analysis was performed to create models for predicting the CPRs of each etiological group.Results: The overall CPR was 13.3%. There were significant improvements for most sperm parameters after DGC. Multivariate logistic regression analysis indicated that, in overall AIH cases, the top parameters significantly influencing the CPR of AIH were pre-STR (OR = 1.037; P = 0.048) and post-VSL (OR = 1.036; P = 0.011). In the Male-factor Group, the top influencing parameters were pre-VCL (OR = 2.096; P = 0.008), pre-LIN (OR = 1.930; P = 0.002) and post-VSL (OR = 1.316; P = 0.023). In the Both-factor Group, the top influencing parameters were pre-VCL (OR = 1.451; P = 0.008) and post-motility (OR = 1.218; P = 0.049). In the Other-factor Group, the top influencing parameters were pre-VAP (OR = 1.715; P = 0.024), pre-STR (OR = 1.20; P = 0.011) and post-VSL (OR = 1.04; P = 0.017). Moreover, receiver operating characteristic analysis showed that the logistic regression models of the Male- and Both-factor Groups had greater powers for prognostic classification than those of other groups.Conclusions: This study demonstrated that some sperm parameters have a collinearity relationship in predicting the CPR following AIH. Moreover, the predictive capacity of a multivariate logistic regression model is better than those of individual parameters, especially for the Male- and Both-factor Groups. In these cases, pre-VCL is the common top influencing factor. [ABSTRACT FROM AUTHOR]

Abstract: Polychlorinated biphenyls (PCBs) are still prevalent in the environment despite the fact that they have been banned in many countries for several decades. Recent epidemiologic studies have demonstrated a link between PCBs exposure and pathological alterations of bone tissues. The aim of this study was to investigate the toxic effects of the PCBs mixture Aroclor 1254 on MC3T3-E1 preosteoblasts and explore the underlying molecular mechanism. Different doses of Aroclor 1254 were used to treat MC3T3-E1 and the cell viability, apoptosis, ALP activity, intracellular calcium (Ca2+) level and oxidative stress response were measured. The expression level of related proteins TRPV6, Apaf-1 and Bax was evaluated with Western blot assay. The subcellular distribution of TRPV6 protein was detected with immunofluorescence assay. The results indicated that the higher dose of Aroclor 1254 (>10mg/L) could inhibit the cell proliferation and induce apoptosis in MC3T3-E1. The ROS level following Aroclor 1254 exposure was elevated with the concentration, while the ALP activity and intracellular calcium (Ca2+) level decreased. After Aroclor 1254 exposure, the expression level of calcium transport related protein TRPV6 was down-regulated, while the expression level of apoptosis related proteins Apaf-1 and Bax up-regulated in a dose dependant manner. The immunofluorescence assay results showed that the expression of TRPV6 in the cytoplasm was greatly suppressed after Aroclor 1254 exposure. In conclusion, Aroclor 1254 exposure could induce toxic effects in MC3T3-E1 as evidenced by inhibition of proliferation, induction of apoptosis and suppression of ALP activity. The ROS production and alteration of intracellular Ca2+ level induced by down-regulation of TRPV6 might involve the toxic effects, and cell apoptosis induced by Aroclor 1254 exposure is associated with the pro-apoptotic Apaf-1 pathway as well as alteration of Bcl-2/Bax ratio. [Copyright &y& Elsevier]

Abstract: Polybrominated diphenyl ethers (PBDEs) had been used extensively in electrical and electronic products as brominated flame retardants. PBDEs are widely distributed in environment media and wildlife since they are lipophilic and persistent, resulting in bioaccumulation and bioamplification through food chains. Accumulation of PBDEs in the environment and human tissues will consequently cause potential negative effects on the ecological environment and human health. To date, some in vitro and in vivo studies have reported that PBDEs possess neurotoxicity, hepatotoxicity, immunotoxicity, reproduction toxicity, endocrine disrupting activity and carcinogenicity. BDE-47 is one of the most predominant PBDE congeners detected in human tissues. The objective of this study is to investigate whether low concentration of BDE-47 could cause hormesis effect in the human hepatoma HepG2 cells, and to explore the possible molecular mechanism. The results showed that low concentration of BDE-47 (10−10, 10−9 and 10−8 M) could promote cell proliferation and cause no obvious change in DNA damage or cell apoptosis, while the high concentration significantly inhibit cell proliferation. Meanwhile, the reactive oxygen species (ROS) in low concentration BDE-47 (10−10, 10−9 and 10−8 M) treated groups significantly elevated compared with the control group. After low concentration BDE-47 treatment, the expression of proliferating cell nuclear antigen (PCNA), Cyclin D1, DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and phosphorylated protein kinase B (p-Akt) in the HepG2 cells was markedly up-regulated. However, in DNA-PKcs inhibited cells, the promotion effect on cell proliferation was significantly suppressed. Cell cycle analysis showed a significant decrease in G1 phase after exposure to low concentration of BDE-47. Moreover, pre-exposure to low concentration BDE-47 seemed alleviate the negative effects of high concentration (50μM) exposure to cause DNA damage and apoptosis. These results suggested that BDE-47 has a hormesis effect in HepG2 cells and DNA-PKcs/Akt pathway may be involved in regulation of cell proliferation and apoptosis. [Copyright &y& Elsevier]

Graphical abstract Highlights • MSWI PM 2.5 presents significantly higher cytotoxicity than Biomass PM 2.5. • The chemical heterogeneity determines the toxic endpoints of MSWI PM 2.5. • Cytotoxicity is mostly attributable to the insoluble fractions. • Biomass PM 2.5 shows a significant pro-inflammatory potential. Abstract Fine particles (PM 2.5) emitted from municipal solid waste incineration (MSWI) contain high amounts of toxic compounds and pose a serious threat to environment and human health. In this study, entire particles as well as extracted water-soluble and -insoluble fractions of PM 2.5 collected from MSWI and biomass incineration (BMI) were subjected to physiochemical characterization and cytotoxic tests in A549 and BEAS-2B cells. MSWI PM 2.5 had higher contents of heavy metals (including Pb, Zn, and Cu) and dioxins (PCDD/Fs) than did BMI PM 2.5. The metals were enriched in the water-insoluble fraction, as measured by inductively coupled plasma-atomic emission spectrometry. BMI PM 2.5 had a higher content of endotoxin, which was also enriched in the water-insoluble fraction. MSWI PM 2.5 caused more serious cell injuries, as indicated by the lower viability, higher ROS generation, and DNA damage, whereas BMI PM 2.5 presented higher pro-inflammatory potential, as indicated by increased mRNA levels of interleukin 6. Normal human BEAS-2B cells were more sensitive than A549 cells in all these tests. Toxic effects caused by MSWI and BMI PM 2.5 were mostly attributable to their water-insoluble fractions. Our results indicate different chemical and biological compositions in MSWI and BMI PM 2.5 probably dominate in different toxic endpoints in vitro. [ABSTRACT FROM AUTHOR]

Abstract After emitted from incomplete combustion of fossil fuels and biomass, ambient black carbon (BC) was then undergone photochemical oxidization processes in the air to form aged BC particles, also called oxidized BC (OBC). This study aimed to investigate the interactions between oxidative stress, autophagy and apoptosis induced by OBC in A549 cells and to explore associated molecular mechanisms. First, OBC could stimulate oxidative stress, autophagy and apoptosis dose-dependently, as evidenced by increased intercellular reactive oxygen species (ROS) levels, up-regulated autophagosome markers (light chain 3, LC3), and elevated apoptosis rate. Inhibitors of oxidative stress (N -acetylcysteine, NAC), autophagy (bafilomycin A1, Baf) and apoptosis (Z -DEVD-FMK) were used to investigate their interactions. NAC pretreatment could significantly reduce autophagy and apoptosis. Additionally, pretreatment with Baf or Z -DEVD-FMK could also significantly suppress the other two biological effects. Furthermore, OBC up regulated the expressions of DNA-dependent protein kinase catalytic subunit (DNA-PKcs), phosphorylated protein kinase B (Akt) and mammalian target of rapamycin (mTOR). The Akt inhibitor (MK-2206) significantly reduced both autophagy and apoptosis. Taken together, dual-direction regulation existed between each two of oxidative stress, autophagy, and apoptosis in A549 cells exposed to OBC. In addition, the autophagy process is modulated by the PI3K/Akt pathway regardless of mTOR activity. Graphical abstract Unlabelled Image Highlights • Oxidized BC containing PAHs activated autophagy, apoptosis and oxidative stress in A549 cells. • Dual-direction regulations existed between autophagy and apoptosis. • Autophagy and apoptosis were regulated by PI3K/Akt pathway. • Autophagy and apoptosis were independent of mTOR pathway [ABSTRACT FROM AUTHOR]

Ambient particulate matter (PM) is a worldwide health issue of concern. However, limited information is available regarding the toxic contributions of the nitro-derivatives of polycyclic aromatic hydrocarbons (nitro-PAHs). This study intend to examine whether 1-nitropyrene (1-NP) and 3-nitrofluoranthene (3-NF) could activate the nuclear factor-erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) antioxidant defense system, and whether the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway participates in regulating pro-inflammatory responses in A549 cells. Firstly, 1-NP and 3-NF concentration-dependently induced cellular apoptosis, reactive oxygen species (ROS) generation, DNA damage, S phase cell cycle arrest and differential expression of related cytokine genes. Secondly, 1-NP and 3-NF activated the Nrf2/ARE defense system, as evidenced by increased protein expression levels and nuclear translocation of transcription factor Nrf2, elevated Nrf2/ARE binding activity, up-regulated expression of the target gene heme oxygenase-1 (HO-1). Significantly increased protein expression of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and phosphorylation level of Akt indicated that the PI3K/Akt pathway was activated during pro-inflammatory process. Further, both PI3K inhibitor (LY294002) and Akt inhibitor (MK-2206) reversed the elevated TNF-α expression to control level. Our results suggested that Nrf2/ARE pathway activation might cause an initiation step in cellular protection against oxidative stress caused by nitro-PAHs, and the PI3K/Akt pathway participated in regulating inflammatory responses. [ABSTRACT FROM AUTHOR]

Oral ingestion plays an important role in human exposure to polybrominated diphenyl ethers (PBDEs). The uptake of PBDEs primarily occurs in the small intestine. The aim of the present study is to investigate the transepithelial transport characteristics and mechanisms of PBDEs in the small intestine using a Caco-2 cell monolayer model. The apparent permeability coefficients of PBDEs indicated that tri- to hepta-BDEs were poorly absorbed compounds. A linear increase in transepithelial transport was observed with various concentrations of PBDEs, which suggested that passive diffusion dominated their transport at the concentration range tested. In addition, the pseudo-first-order kinetics equation can be applied to the transepithelial transport of PBDEs. The rate-determining step in transepithelial transport of PBDEs was trans-cell transport including the trans-pore process. The significantly lower transepithelial transport rates at low temperature for bidirectional transepithelial transport suggested that an energy-dependent transport mechanism was involved. The efflux transporters (P-glycoprotein, multidrug resistance-associated protein, and breast cancer resistance protein) and influx transporters (organic cation transporters) participated in the transepithelial transport of PBDEs. In addition, the transepithelial transport of PBDEs was pH sensitive; however, more information is required to understand the influence of pH. [ABSTRACT FROM AUTHOR]

In order to clarify the cytotoxicity of hexabromocyclododecane (HBCD) diastereoisomers, and to investigate the correlation of cytotoxicity and biotransformation of HBCDs, the immortalized human liver cells L02 and human hepatoma cells HepG2 were exposed to individual HBCD diastereoisomer (α-, β- and γ-HBCD). Cytotoxicity was assayed in terms of cell viability, reactive oxygen species (ROS) level and DNA damage. Metabolic rate, bioisomerization and enantiomer fractions were analyzed using the liquid chromatograph coupled to triple quadrupole mass spectrometer (LC-MS/MS). The α-, β- and γ-HBCD all had cytotoxicity in L02 and HepG2 cells with the toxicity order β-HBCD ≥ γ-HBCD > α-HBCD according to the results of proliferation assay. The cytotoxicity mechanism between the two cells seemed different: a) the stability of intracellular redox state plays an important role in inducing cell toxicity in HepG2 cells. b) DNA damage status is central to inhibit proliferation in L02 cells. The metabolic capability of HepG2 was superior to L02 for HBCD diastereoisomers, which may explain the greater toxicity of HBCDs in HepG2 cells. The bioisomerization and enantiomer enrichment were also detected in this study, although the results were inconsistent with other reports, which might result from species-specific differences in HBCDs metabolism or experimental conditions. The cytotoxicity and metabolic mechanism of individual enantiomers must be further investigated to evaluate the health risks of HBCDs. [ABSTRACT FROM AUTHOR]

In order to elucidate the cytotoxicity of organophosphate flame retardants (OPFRs), three human in vitro models, namely the HepG2 hepatoma cells, the A549 lung cancer cells and the Caco-2 colon cancer cells, were chosen to investigate the toxicity of triphenyl phosphate (TPP), tributylphosphate (TBP), tris(2-butoxyexthyl) phosphate (TBEP) and tris (2-chloroisopropyl) phosphate (TCPP). Cytotoxicity was assayed in terms of cell viability, DNA damage status, reactive oxygen species (ROS) level and lactate dehydrogenase (LDH) leakage. The results showed that all these four OPFRs could inhibit cell viability, overproduce ROS level, induce DNA lesions and increase the LDH leakage. In addition, the toxic effects of OPFRs in Caco-2 cells were relatively severer than those in HepG2 and A549 cells, which might result from some possible mechanisms apart from oxidative stress pathway. In conclusion, TBP, TPP, TBEP and TCPP could induce cell toxicity in various cell lines at relatively high concentrations as evidenced by suppression of cell viability, overproduction of ROS, induction of DNA lesions and increase of LDH leakage. Different cell types seemed to have different sensitivities and responses to OPFRs exposure, as well as the underlying potential molecular mechanisms. [ABSTRACT FROM AUTHOR]

A facile vesicle-templating approach has been developed for synthesis of multi-shelled mesoporous silica nanoparticles (MMSNs) through a self-assembly of cetyltrimethylammonium bromide (CTAB) and sodium dodecyl benzene sulfonate (SDBS). The obtained MMSNs displayed a spherical morphology, relatively uniform size distribution with an average diameter of 185 nm and a good biocompatibility. Controlled experiments demonstrated that the morphology and structure of MMSNs were mainly determined by the mass ratio of CTAB/SDBS in the reagents. A possible growth mechanism of MMSNs was proposed based on TEM, SEM, and N 2 sorption analysis, etc. Moreover, the Au-decorated MMSNs (Au@MMSNs) were constructed as the catalyst, which exhibited superior catalytic activity and good cycle stability for the reduction of 4-nitrophenol (4-NP). Additionally, the MMSNs also showed high drug loading efficiency and the controlled pH-responsive release behavior for doxorubicin hydrochloride (DOX). More importantly, the anticancer effect of DOX@MMSNs towards A549 cell further confirmed MMSNs could be employed as an ideal drug carrier. As a consequence, the MMSNs prepared are potential excellent candidates for various applications including nanoreactors, drug delivery, and cancer therapy. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the “adaptive responses” of hexabromocyclododecanes (HBCD) at environmentally relevant concentrations in human hepatocytes L02. L02 cells were pre-treated with low concentrations of HBCD (10 −13 –10 −11 M), followed by treatment with high concentrations of HBCD, α-hexachlorocyclohexane (α-HCH), polychlorinated biphenyls (PCBs), or polybrominated diphenyl ether-47 (BDE47). The results showed that the pre-treatment with low concentrations of HBCD induced “adaptive responses” to high concentrations of HBCD/α-HCH exposure (but not to PCBs and BDE47), as evidenced by attenuation of survival inhibition, reactive oxygen species (ROS) over-production, and deoxyribonucleic acid (DNA) damage induction. The “adaptive responses” induced by low concentrations of HBCD, which depended on the activation of the phosphatidylinositide 3-kinase/protein kinase B (PI3K/Akt) pathway, reduced the phosphorylation of adenosine monophosphate-activated kinase (AMPK) and enhanced the phosphorylation of p38 mitogen-activated protein kinases (p38 MAPK). The observations were further confirmed by the experiments with inhibitors. Moreover, the evaluation on the changes of metabolic enzymes revealed that HBCD and α-HCH shared a similar pattern of cytochrome P450 induction (CYP2B6), which was different from those of PCBs and BDE47 (CYP1A1 and CYP2B6). These results indicated that low concentrations of HBCD could induce “adaptive responses” to the subsequent treatment with high concentrations of HBCD/α-HCH in L02 cells, which was associated with the PI3K/Akt pathway, and AMPK and p38 MAPK signaling. The “adaptive responses” seemed to be dependent on the types of chemicals in terms of the metabolic patterns and chemical structures. [ABSTRACT FROM AUTHOR]

Highlights: [•] HBCD induced obvious oxidative damage in HepG2 cells. [•] OPCs could effectively protect cells against HBCD-induced cytotoxicity. [•] ROS formation, mitochondrial pathway, and Ca2+ level are involved in OPCs effect regulation. [ABSTRACT FROM AUTHOR]

Electrical and electronic waste (E-waste) has now become the fastest growing solid waste around the world. Primitive recycling operations for E-waste have resulted in severe contamination of toxic metals and organic chemicals in the related areas. In this study, six dust and soil samples collected from E-waste recycling workshops and open-burning sites in Longtang were analyzed to investigate their cytotoxicity and genotoxicity on L02 cells. These six samples were: dust No. 1 collected at the gate of the workshop; dust No. 2 collected from air conditioning compressor dismantling site; dust No. 3 collected from where some motors, wires, and aluminium products since the 1980s were dismantled; soil No. 1 collected at the circuit board acid washing site; soil No. 2 collected from a wire open-burning site; soil No. 3 collected near a fiber open-burning site. At the same time, two control soil samples were collected from farmlands approximately 8 km away from the dismantling workshops. The results showed that all of these samples could inhibit cell proliferation and cause cell membrane lesion, among which dust No. 3 and soil No. 2 had the strongest toxicity. Moreover, the comet assay showed that the dust No. 3 had the most significant capability to cause DNA single-strand beaks (SSB), while the road dust (dust No. 1) collected at the gate of the workshop, a relatively farer site, showed the slightest capability to induce DNA SSB. The intracellular reactive oxygen species (ROS) detection showed that ROS level was elevated with the increase of dust and soil samples concentration. Dust No. 3 and soil No. 2 had the highest ROS level, followed by dust No. 2 and 1, soil No. 3 and 1. All of the above results indicated that polluted soil and dust from the E-waste area had cytotoxicity and genotoxicity on L02 cells, the mechanism might involve the increased ROS level and consequent DNA SSB. [ABSTRACT FROM PUBLISHER]

Abstract: Polybrominated diphenyl ethers (PBDEs) and polycyclic aromatic hydrocarbons (PAHs) coexist widely in the environment and have generated adverse effects on the environment and human health. The purpose of this study was to investigate the combined toxic effects of these chemicals and the related mechanism. L02 cells were exposed to BDE47 (5, 10μmol/L) or/and BaP (50μmol/L) in different administration order. The cell growth and survival, DNA strand breaks, oxidative stress index (ROS, SOD, GSH, and MDA), LDH release and the expression level of CYP1 family members were measured. The result showed that BDE47 or/and BaP had no effect on the cell growth and survival under the present conditions. However, compared with the groups treated with BDE47 or BaP alone, the combined-treated groups induced significantly elevated DNA strand breaks, ROS production, and MDA level. Especially, pretreatment with BDE47 followed by BaP led to the strongest effects. Addition of the antioxidant N-acetyl-l-cysteine (NAC) markedly reduced the ROS level and partly suppressed the DNA strand breaks induced by BDE47 or/and BaP. Meanwhile, the combined treatment groups also markedly increased the SOD activity, GSH content, and LDH release level compared with the control group. The real-time PCR results showed that BaP could significantly induce the expression of CYP1A1 and CYP1B1, however, the pre-treatment with BDE47 appeared to attenuate the BaP-induced CYP1 expression. All of above findings indicated that BDE47 and BaP had a synergistic effect on oxidatively generated DNA damage in L02 cells via regulation on the oxidative stress response and the expression of CYP1 metabolism enzymes. [Copyright &y& Elsevier]