Fine particulate-bound arsenic and selenium from coal-fired power plants: Formation, removal and bioaccessibility.

The arsenic (As) and selenium (Se) in fine particulate matter (PM10) have attracted increasing attentions due to their health effects. However, the emission control of fine particulate-bound arsenic and selenium (fine particulate-bound As/Se) from coal-fired power plants still faces various challenges. Understanding the formation and characteristics of fine particulate-bound As/Se is crucial for developing specific control technologies. This study clarifies the formation mechanism, removal characteristics, and inhalation bioaccessibility of fine particulate-bound As/Se from industrial coal-fired power plants through methods including aerosol generation, As/Se speciation determination, and in vitro bioaccessibility testing. The findings demonstrated that PM1 from pulverized coal-fired (PC) boilers was enriched with As/Se in terms of concentration and mass distribution. Instead, As/Se was mainly distributed in PM2.5-10 from circulating fluidized bed (CFB) boilers. Limestone injection in CFB boilers promoted As/Se enrichment in coarse PM. Fine particulate-bound As was mainly formed by chemical adsorption of As vapors by Ca-minerals, while the formation of fine particulate-bound Se was closely related to active Ca-minerals and Fe-minerals. Furthermore, Ca-bound As was easy to remove by electrostatic precipitator (ESP) and the removal of physically adsorbed SeO2(s) was difficult, which was caused by the specific resistivity of different mineral components. Importantly, finer particulate-bound As/Se posed higher inhalation bioaccessibility, following the order of PM1 ≥ PM1-2.5 > PM2.5-10. In particular, Ca-bound Se in fine PM owned high bioaccessibility. Based on these findings, measures were proposed to suppress the formation of fine particulate-bound As/Se in the furnace and/or strengthen its removal in the post-combustion stage.

Remediation of hexachlorobenzene-contaminated soils with alkyl glycoside-enhanced desorption and zero-valent iron-EDTA-air treatment.

In this work, the use of a coupled process, alkyl glycoside (APG) enhanced soil desorption followed by the zero-valent iron-ethylenediaminetetraacetic acid (EDTA)-air (ZEA) Fenton-like system, was investigated for the remediation of a simulated hexachlorobenzene (HCB)-contaminated diatomite soil and a real HCB-contaminated soil. Three surfactants with different concentrations were studied to obtain the suitable soil desorption agent. Compared with APG0810 and Triton x-100, APG0814 showed a better solubilization effect due to its lower critical micelle concentration. With addition of 3000 mg L-1 APG0814, 35% of HCB was removed from contaminated diatomite soil, and a small amount of residual APG in diatomite soil was found to be beneficial for the soil dispersion. After treatment with the ZEA system, the removal efficiency of HCB in the diatomite soil desorption solution reached 76% in 2 h; we observed that a small amount of APG retained in the desorption solution accelerated the HCB removal. A real HCB-contaminated soil was used to verify the remediation effects. This study demonstrates that our approach is a feasible alternative for remediating soil contaminated with hydrophobic organic compounds.

Stabilization treatment of arsenic-alkali residue (AAR): Effect of the coexisting soluble carbonate on arsenic stabilization.

Arsenic-alkali residue (AAR) from antimony smelting is highly hazardous due to its ready leachability of As, seeking for proper disposal such as stabilization treatment. However, As stabilization in AAR would be challenging due to the high content of coexisting soluble carbonate. This study conducted the stabilization treatments of AAR by ferrous sulfate and lime, respectively, and revealed the significant influence of coexisting carbonate. It was found that ferrous sulfate was more efficient than lime, which required only one-tenth of dosages of lime to reduce the As leaching concentration from 915 mg/L to a level below 2.5 mg/L to meet the Chinese regulatory limit. The combining qualitative and quantitative analyses based on XRD, SEM-EDS, and thermodynamic modeling suggested that the formation of insoluble arsenate minerals, ferrous arsenate or calcium arsenate, was the predominant mechanism for As stabilization in the two treatment systems, and their efficiency difference was primarily attributed to the coexisting carbonate, which had a slight effect on ferrous arsenate but severely obstructed calcium arsenate formation. Moreover, the examination of As leaching concentrations in 1-year-cured samples indicated that the long-term stability of ferrous sulfate treatment was far superior to that of lime treatment. This study provides ferrous salts as a promising and green scheme for stabilization treatment of AAR as well as other similar As-bearing solid wastes with coexisting soluble carbonate.

Matrine suppresses breast cancer metastasis by targeting ITGB1 and inhibiting epithelial-to-mesenchymal transition.

Metastasis can be a fatal step in breast cancer progression. Effective therapies are urgently required due to the limited therapeutic options clinically available. The aim of the present study was to investigate the effect of matrine (MAT), a traditional Chinese medicine, on the proliferation and migration of human breast cancer cells and its underlying mechanisms of action. The proliferation of MDA-MB-231 cells was inhibited and apoptosis was induced following treatment with MAT, as determined by MTT and Annexin-V-FITC/PI assays. Western blot analysis was used to detect the LC-3II/I levels and the results suggested that tumor autophagy is involved in the anti-tumor activity of MAT. To the best of our knowledge, this is the first study to report that MAT inhibits MDA-MB-231 and MCF-7 cell motility, potentially by targeting integrin ß1 (ITGB1) and epithelial-to-mesenchymal transition (EMT), as indicated by Transwell® and siRNA interference assays. In conclusion, ITGB1 and EMT are involved in MAT-induced breast carcinoma cell death and the inhibition of metastasis. This may lead to the development of novel compounds for the treatment of breast cancer metastasis.

Ethyl acetate extract from Inula helenium L. inhibits the proliferation of pancreatic cancer cells by regulating the STAT3/AKT pathway.

Sesquiterpene lactones are bioactive compounds that have been identified as responsible for the anticancer activity of the medicinal herb, Inula helenium L. (IHL). However, the mechanisms of action involved in the anti­pancreatic cancer activity of IHL have yet to be elucidated. The present study used an optimized extraction strategy to obtain sesquiterpene lactones from IHL (the resulting product termed ethyl acetate extract of IHL; EEIHL), and examined the potential mechanisms involved in the anti­pancreatic cancer activity of EEIHL. Ethanol and ethyl acetate were used to extract sesquiterpene lactones from IHL to give the final product EEIHL. Cell Counting Kit­8, colony formation and Annexin V/propidium iodide assays were used to detect the anti­proliferative activity of EEIHL. Cell migration was determined with a wound healing assay. mRNA and protein expression levels were analyzed by reverse transcription­quantitative polymerase chain reaction and western blot analyses, respectively. It was identified that low concentrations of EEIHL caused CFPAC­1 cell cycle arrest in the G0/G1 phase, whereas high concentrations of EEIHL induced mitochondria­dependent apoptosis. In addition, EEIHL could inhibit the phosphorylation of the signal transducer and activator of transcription (STAT)3/AKT pathway, potentially resulting in impeded cell mobility. In conclusion, EEIHL could activate mitochondrial­dependent apoptosis and inhibit cell migration through the STAT3/AKT pathway in CFPAC-1 cells.

Deacetylisovaltratum disrupts microtubule dynamics and causes G2/M-phase arrest in human gastric cancer cells in vitro.

AIM: Deacetylisovaltratum (DI) is isolated from the traditional Chinese herbal medicine Patrinia heterophylla Bunge, which exhibits anti-cancer activity. Here, we investigated the effects of DI on human gastric carcinoma cell lines in vitro and elucidated its anti-cancer mechanisms. METHODS: Human gastric carcinoma AGS and HGC-27 cell lines were treated with DI, and cell viability was detected with MTT assay. Cell cycle stages, apoptosis and mitochondrial membrane potential were measured using flow cytometry. Protein levels were analyzed by Western blotting. Tubulin polymerization assays and immunofluorescence were used to characterize the tubulin polymerization process. RESULTS: DI inhibited the cell viability of AGS and HGC-27 cells in a dose- and time-dependent manner with IC50 values of 12.0 and 28.8 µmol/L, respectively, at 24 h of treatment. Treatment with DI (10-100 µmol/L) dose-dependently promoted tubulin polymerization, and induced significant G2/M cell cycle arrest in AGS and HGC-27 cells. Moreover, DI treatment disrupted mitochondrial membrane potential and induced caspase-dependent apoptosis in AGS and HGC-27 cells. CONCLUSION: DI induces G2/M-phase arrest by disrupting tubulin polymerization in human gastric cancer cells, which highlights its potent anti-cancer activity and potential application in gastric cancer therapy.