[Identification of Impacts from Meteorology and Local and Transported Photochemical Generation on Ozone Trends in Changsha from 2018 to 2020].

Ozone (O3) pollution in Hunan province has become the most important factor among the six common conventional pollutants (i.e., NO2, SO2, CO, O3, PM10, and PM2.5) in the atmospheric environment. Further investigation has indicated that the relevant studies of O3 are insufficient. Therefore, it is essential to clarify the key driving factors of O3 variations for government regulators. In this study, a combined method consisting of a generalized additive model (GAM), empirical orthogonal function (EOF), and absolute principal component scores (APCs) model was employed to identify and quantify the impacts of meteorology and local photochemical generation (local) and that transported from outside (nonlocal) on O3 variations from 2018-2020. Simultaneously, the driving factors of O3 annual values from 2018 to 2019 and from 2019 to 2020 in Changsha were analyzed. The results showed that O3 episodes were commonly caused by meteorology when the relative contribution from precursors was high, on the short-term time scale. Overall, on the temporal scale, meteorology and local were the driving factors for the increasing annual O3 from 2018 to 2019. Additionally, the contribution from meteorology, local, and nonlocal decreased from 2019 to 2020, leading to a lower level of O3 concentration in 2020. Geographically, the east, north, and south of Changsha were mainly affected by meteorology, local, and nonlocal, respectively. Throughout the three years, nonlocal exhibited a sustained decreasing trend, whereas the tendencies from meteorology and local varied by year and geography. Local contribution in the north of Changsha increased from 2018 to 2019, which was likely attributed to the increasing biogenic volatile organic compound emission (BVOCs), and it became lower in the south owing to the strengthened consumption by NOx. Impacts from meteorology on O3 in all sites were enhanced from 2018 to 2019. By contrast, local contribution decreased in the north and increased in the south with the decline in BVOC and NOx emissions from 2019 to 2020, when the meteorological impacts on O3 in the whole area became weak.

Peroxiredoxin 5 protects HepG2 cells from ethyl ß-carboline-3-carboxylate-induced cell death via ROS-dependent MAPK signalling pathways.

Peroxiredoxin 5 (PRDX5) is the member of Prxs family, widely reported to be involved in various types of cell death. We previously found that PRDX5 knockdown increases the susceptibility of cell death upon oxidative stress treatment. Ethyl ß-carboline-3-carboxylate (ß-CCE), an alkaloid extracted from Picrasma quassioides, has been reported to play a role in neuronal disease, but its anti-cancer potential on liver cancers remains unknown. Here, we studied the effect of PRDX5 on ethyl ß-carboline-3-carboxylate (ß-CCE)-induced apoptosis of hepatomas. High expression level of PRDX5 was deeply related with the postoperative survival of patients with liver cancer, indicating that PRDX5 may be a biomarker of live cancer processing. Moreover, PRDX5 over-expression in HepG2 cells significantly inhibited ß-CCE-induced cell apoptosis and cellular ROS levels as well as mitochondrial dysfunction. Signalling pathway analysis showed that ß-CCE could significantly up-regulate the ROS-dependent MAPK signalling, which were in turn boosts the mitochondria-dependent cell apoptosis. Moreover, PRDX5 over-expression could reverse the anti-cancer effects induced by ß-CCE in HepG2 cells. Our findings suggest that PRDX5 has a protective role on ß-CCE-induced liver cancer cell death and provides new insights for using its anti-cancer properties for liver cancer treatment.

[Pollution Characteristics and Emission Factors of PCDD/Fs from Iron and Steel Industry].

The pollution level, emission characteristics, and emission factors of PCDD/Fs from a number of steel plants were investigated in a particular province of China. The results showed that the concentration of PCDD/Fs was at a low level and decreased by 1-2 orders of magnitude compared with that in 2005-2019. In detail, the concentrations of PCDD/Fs ranged from 0.003-0.557 ng·m-3(I-TEQ), and the mean value was 0.165 ng·m-3 for the sintering process. Moreover, the concentrations of PCDD/Fs ranged from 0.006 to 0.057 ng·m-3, and the mean value was 0.025 ng·m-3 for the electric furnace process. In addition, the concentration of PCDD/Fs in the iron and steel industry from 2005 to 2020 increased first and then decreased, especially after the implementation of the new emission standard and the ultra-low emission control of conventional pollutants such as smoke, showing a significant decline. The results of fingerprint analysis showed that 2,3,7,8-TCDF was the largest congener contributing to the mass concentration, and lower chlorinated PCDFs were increased. This result differed from those of previous studies in which highly chlorinated PCDFs and PCDDs dominated, indicating that the generation source of PCDD/Fs had changed. The congener and isomer profiles of PCDD/Fs in flue gas from the sintering process were similar to those in the flue gas from the electric furnace process. Additionally, showing the characteristics of the typical high-temperature thermal process, the de novo synthesis may be the dominant mechanism of formation of PCDD/Fs in the sintering process and electric furnace process. The emission factor was 0.003-0.5 µg·t-1 (I-TEQ), and the average emission factor was (0.18±0.22) µg·t-1 for the sintering process. The emission factor was 0.04-0.5 µg·t-1, and the average emission factor was (0.27±0.23) µg·t-1 for the electric furnace process. These values were far lower than those of the standard toolkit for identification and quantification of dioxin and furan emissions released by UNEP in 2013 and the emission factors in the dioxin emission inventory of China in 2004. It is suggested that the emission factors of PCDD/Fs in the iron and steel industry of China should be studied and updated.

Knockdown of Peroxiredoxin V increased the cytotoxicity of non-thermal plasma-treated culture medium to A549 cells.

Administration of non-thermal plasma therapy via the use of plasma-activated medium (PAM) might be a novel strategy for cancer treatment, as it induces apoptosis by increasing reactive oxygen species (ROS) levels. Peroxiredoxin V (PRDX5) scavenges ROS and reactive nitrogen species and is known to regulate several physiological and pathological reactions. However, its role in lung cancer cells exposed to PAM is unknown. Here, we investigated the effect of PRDX5 in PAM-treated A549 lung cancer cells and determined the mechanism underlying its cytotoxicity. Cell culture medium was treated with low temperature plasma at 16.4 kV for 0, 60, 120, or 180 s to develop PAM. PRDX5 was knocked down in A549 cells via transfection with short hairpin RNA targeting PRDX5. Colony formation and wound healing assays, flow cytometry, fluorescence microscopy, and western blotting were performed to detect the effect of PRDX5 knockdown on PAM-treated A549 cells. PAM showed higher cytotoxicity in lung cancer cells than in control cells, downregulated the mitogen-activated protein kinase signaling pathway, and induced apoptosis. PRDX5 knockdown significantly inhibited cell colony formation and migration, increased ROS accumulation, and reduced mitochondrial membrane potential in lung cancer cells. Hence, PRDX5 knockdown combined with PAM treatment represents an effective option for lung cancer treatment.

Ethyl ß-Carboline-3-Carboxylate Increases Cervical Cancer Cell Apoptosis Through ROS-p38 MAPK Signaling Pathway.

BACKGROUND/AIM: Ethyl ß-carboline-3-carboxylate (ß-CCE) is one of the effective ingredients of Picrasma quassioides (P. quassioides). As a ß-carboline alkaloid, it can antagonize the pharmacological effects of benzodiazepines by regulating neurotransmitter secretion through receptors, thus affecting anxiety and physiology. However, its efficacy in cancer treatment is still unclear. MATERIALS AND METHODS: We explored the effect of b-CCE on SiHa cells using MTT assay, western blot, flow cytometry, LDH release, T-AOC, SOD, and MDA assays. RESULTS: We investigated the cytotoxicity of ß-CCE in SiHa cells and verified that ß-CCE could induce cell apoptosis in a time- and concentration-dependent manner. In this process, treatment with ß-CCE significantly increased the levels of cytoplasmic and mitochondrial reactive oxygen species (ROS), which disturb the oxidation homeostasis by regulating the total antioxidant capacity (T-AOC), superoxide dismutase (SOD) activity, and malondialdehyde (MDA) production. Notably, the addition of N-acetylcysteine (NAC) (ROS scavenger) effectively alleviated ß-CCE-induced apoptosis in SiHa cells. In addition, ß-CCE might activate the p38/MAPK signaling pathway, as the pre-treatment with SB203580 (p38 inhibitor) significantly reduced ß-CCE-induced apoptosis in SiHa cells. CONCLUSION: ß-CCE has an anti-tumor activity. It activates the p38/MAPK signaling pathway by increasing intracellular ROS levels, which subsequently induce SiHa cell apoptosis. Our results provide a novel therapeutic target for treatment of cervical cancer.

[Analysis of Ozone Pollution Spatio-temporal Evolution Characteristics and Identification of Its Long-term Variation Driving Factor over Hunan Province].

Despite the alleviation of particulate matter (PM), the ambient ozone (O3) concentration is continuously increasing in Hunan province where the investigation of O3 pollution has been rarely reported. Accordingly, the spatio-temporal evolution of O3 pollution was first analyzed based on hourly air quality data observed by national monitoring stations from 2015 to 2020 over 14 cities in Hunan province. Afterwards, the combination of meteorological data from the European Center for Medium-range Weather Forecast (ECMWF) and the generalized additive model (GAM) was applied to investigate the driving factors of the O3 long-term trend during this period. The results presented obvious diurnal, monthly, and seasonal characteristics of O3 variations. High O3 concentrations occurred in May and September monthly, and the peak O3 season was autumn. Furthermore, the 90th percentile O3 increased at a rate of 4.7 µg·(m3·a)-1 temporally, and high O3 values mainly occurred in the north-eastern region spatially, in contrast to the low O3 values in the western region. The modeling results indicated that the increase in O3 was mainly ascribed to precursor emissions. Furthermore, meteorology promoted a rise in O3 with the impact magnitude of 1 µg·(m3·a)-1. Remarkably, meteorology accelerated the O3 increases in spring, summer, and the eastern region, whereas it restrained increases in autumn, winter, and the northwest. The effect of meteorology on PM10 was different from O3 during this period. Overall, this study highlighted the importance of meteorological impacts when regulating emission reduction measures for O3 abatement. It required greater effort regarding O3 mitigation to offset the side-effect from meteorology in meteorology-sensitive seasons and regions. Additionally, the regional corporation is indispensable to reduce O3 transportation from upwind.

[Pollution Characteristics and Risk Assessment of Nitrated Polycyclic Aromatic Hydrocarbons in the Atmosphere of Guangdong-Hong Kong-Macao Greater Bay Area].

To investigate the pollution characteristics and sources of nitrated polycyclic aromatic hydrocarbons (NPAHs) in Guangdong-Hong Kong-Macao Greater Bay Area (GBA), 44 ambient air samples were collected using the active sampling method, which were then determined via gas chromatography-triple quadrupole tandem mass spectrometry. The main results showed that filters, polyurethane foam, and XAD-2 resin were the essential materials for sampling NPAHs in ambient air in order to characterize the pollution status accurately. The levels of ρ(Σ18NPAHs) in ambient air at GBA ranged from 162 pg·m-3 to 2094 pg·m-3, and the average levels of ρ(Σ18NPAHs) were (675±430) pg·m-3 in summer and (637±349) pg·m-3 in winter. NPAHs were widely found in the ambient air of GBA and were dominated by 1-nitronaphthalene (220 pg·m-3), 2-nitronaphthalene (146 pg·m-3), 9-nitroanthracene (105 pg·m-3), and 2-nitrofluoranthene (72 pg·m-3). The congener profile characteristics of NPAHs in summer and winter were similar. The gas/particle partitioning characteristics of NPAHs revealed that dicyclic and tricyclic NPAHs tend to occur in the gas phase, and tetracyclic NPAHs tend to be adsorbed in the particle phase. The fraction of NPAHs concentrations in the particulate fraction of their total atmospheric concentrations increased with the increase in their molecular weight. In winter, NPAHs tend to be adsorbed in the particle phase, whereas in summer, NPAHs tend to exist in the gas phase. Based on the ratios of characteristic pollutants, in both the summer and winter season, photochemical reactions were the main source of NPAHs in the atmosphere of GBA and were primarily generated by the reaction of the hydroxyl radical in the daytime. The carcinogenic risk value calculation showed that the current carcinogenic risk of NPAHs in the ambient air of GBA was controllable.

[Emission Characteristics and Emission Factors of Volatile Organic Compounds from E-waste Dismantling and Recycling Processes].

A large number of volatile organic compounds (VOCs) are emitted from the high temperature treatment process in the dismantling and recycling procedure of e-wastes, which has a significant impact on the surrounding environment and human health. In this study, an e-waste dismantling and recycling yard was selected to measure the VOCs concentrations and compositions in the exhaust of treatment facilities of heating baking board, plastic granulation, wet extraction, and pyrometallurgical workshops, and the emission characteristics of VOCs and emission factors for total VOCs from different production processes were investigated. The results showed that there were significant differences in total VOCs emission concentrations among different production processes. The concentrations of total VOCs produced in different workshops followed the descending order of the heating baking board (heating rotary plate furnace) process[(2096.1±732.4) µg·m-3] > plastic granulation process[(1639.1±538.5) µg·m-3] > heating baking board (electric heater) process[(625.3±535.5) µg·m-3] > pyrometallurgical process[(436.8±305.2) µg·m-3] > wet extraction process[(271.3±73.1) µg·m-3]. The compositions of VOCs emitted from different production processes were also clearly different; however, the major components of VOCs were generally oxygenated compounds and aromatic hydrocarbons. The specific component characteristics were as follows:the dominant groups of VOCs emitted from the heating baking board process (including heating rotary plate furnaces and electric heaters) were oxygenated compounds and aromatic hydrocarbons, accounting for 74.1%-79.7% of the total. The main components of VOCs emitted from the pelletizing process were aromatic hydrocarbons and oxygenated compounds, accounting for 71.8% of the total. Oxygenated compounds and aromatic hydrocarbons, which contributed equally, were also the main groups of VOCs discharged by the wet extraction process, and the sum proportion of the two groups was 84.2%. Halogenated hydrocarbon was the dominant group of VOCs from the pyrometallurgical process, accounting for 92.1% of the sum of VOCs. There was a substantial divergence in the total VOCs emission factors of different production processes. The ranking of the mean values of emission factors of total VOCs was as follows:the heating baking board (electric heater) process (297.0 g·t-1) > plastic granulation process (29.5 g·t-1) > wet extraction process (25.4 g·t-1) > heating baking board (heating rotary plate furnace) process (25.2 g·t-1) > pyrometallurgical process (1.9 g·t-1). Therefore, the main VOCs emission processes of the e-waste centralized dismantling and recycling industry were the heating baking board process and plastic granulation process.

Pharmacological effects of Picrasma quassioides (D. Don) Benn for inflammation, cancer and neuroprotection (Review).

Picrasma quassioides (D. Don) Benn is an Asian shrub with a considerable history of traditional medicinal use. P. quassioides and its extracts exhibit good therapeutic properties against several diseases, including anti-inflammatory, antibacterial and anticancer effects. However, the composition of compounds contained in P. quassioides is complex; although various studies have examined mixtures or individual compounds extracted from it, studies on the application of P. quassioides extracts remain limited. In the present review, the structures and functions of the compounds identified from P. quassioides and their utility in anti-inflammatory, anticancer and neuroprotectant therapies was discussed. The present review provided up-to-date information on pharmacological activities and clinical applications for P. quassioides extracts.

Anticancer Effect of ERM210 on Liver Cancer Cells Through ROS/Mitochondria-dependent Apoptosis Signaling Pathways.

BACKGROUND/AIM: Asian Traditional medicines are renowned for their antitumor properties and are efficacious in the clinical treatment of various cancer types. ERM210 is a Korean traditional medicine comprising nine types of medicinal plants. In the present study, we examined the pro-apoptotic effect and molecular mechanisms of the effects of ERM210 on HepG2 liver cancer cells. MATERIALS AND METHODS: The cytotoxicity of ERM210 on HepG2 cells was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and wound-healing assays, and apoptosis and signaling pathways by fluorescence microscopy flow cytometry and western blotting. RESULTS: ERM210 significantly impaired HepG2 cell viability and enhanced mitochondria-dependent cellular apoptosis in a time- and dose-dependent manner by up-regulating the expression of caspases 3, 7 and 9, and of BCL2 apoptosis regulator (BCL2)-associated X, apoptosis regulator (BAX) proteins, whilst down-regulating that of BCL2 protein. Furthermore, ERM210 treatment increased accumulation of cellular and mitochondrial reactive oxygen species (ROS) and significantly inhibited cell migration. Additionally, all these phenomena were reversed by treating with the ROS scavenger N-acetylcysteine. The analysis of signaling proteins revealed that ERM210 significantly up-regulated the phosphorylation of ROS-dependent mitogen-activated protein kinases (p38, extracellular-regulated kinase, and c-Jun N-terminal kinase in HepG2 liver cancer cells. CONCLUSION: ERM210 exerts anticancer effects in HepG2 liver cancer cells by up-regulating ROS/mitochondria-dependent apoptosis signaling, providing new insight into the possibility of employing this traditional medicine for the clinical treatment of liver cancer.

Regulatory function of peroxiredoxin I on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung cancer development.

Smoking is a major cause of lung cancer, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is one of the most important carcinogens in cigarette smoke. NNK modulates the expression of peroxiredoxin (Prdx) I in lung cancer. Prdx1 is upregulated in lung squamous cell carcinoma and lung adenocarcinoma, and considered a potential biomarker for lung cancer. The current article reviewed the role and regulatory mechanisms of Prdx1 in NNK-induced lung cancer cells. Prdx1 protects erythrocytes and DNA from NNK-induced oxidative damage, prevents malignant transformation of cells and promotes cytotoxicity of natural killer cells, hence suppressing tumor formation. In addition, Prdx1 has the ability to prevent NNK-induced lung tumor metabolic activity and generation of large amount of reactive oxygen species (ROS) and ROS-induced apoptosis, thus promoting tumor cell survival. In contrast to this, Prdx1, together with NNK, can promote the epithelial-mesenchymal transition and migration of lung tumor cells. The signaling pathways associated with NNK and Prdx1 in lung cancer cells have been discussed in present review; however, numerous potential pathways are yet to be studied. To develop novel methods for treating NNK-induced lung cancer, and improve the survival rate of patients with lung cancer, further research is needed to understand the complete mechanism associated with NNK.

Peroxiredoxin V Silencing Elevates Susceptibility to Doxorubicin-induced Cell Apoptosis via ROS-dependent Mitochondrial Dysfunction in AGS Gastric Cancer Cells.

BACKGROUND/AIM: Peroxiredoxin V (Prx V) plays crucial roles in cellular apoptosis and proliferation in various cancer cells by regulating the cellular reactive oxygen species (ROS) levels. MATERIALS AND METHODS: Here, we examined the possible regulatory effects of Prx V on doxorubicin (DOX)-induced cellular apoptosis and its mechanisms in the human gastric adenocarcinoma cell line (AGS cells). RESULTS: Our findings suggest that Prx V knockdown may significantly increase the DOX-induced apoptosis by aggravating intracellular ROS accumulation. We also found that DOX-induced mitochondrial ROS levels and membrane permeability were significantly higher in short hairpin Prx V cells than in mock cells, and these phenomena were dramatically reversed by ROS scavenger treatment. Prx V knockdown also significantly upregulated the cleaved caspase 9, 3, and B-cell lymphoma 2 (Bcl2)-associated agonist of cell death/Bcl2 protein expression levels, suggesting that Prx V knockdown activates mitochondria-dependent apoptotic signaling pathways. CONCLUSION: Taken together, this study suggests that Prx V may be a strong molecular target for gastric cancer (GC) chemotherapy, and further elucidates the role of Prx V in oxidative stress-induced cell apoptosis.

Curcumin Activates ROS Signaling to Promote Pyroptosis in Hepatocellular Carcinoma HepG2 Cells.

BACKGROUND/AIM: Curcumin is a polyphenol that exerts a variety of pharmacological activities and plays an anti-cancer role in many cancer cells. It was recently reported that gasdermin E (GSDME) is involved in the progression of pyroptosis. MATERIALS AND METHODS: HepG2 cells were treated with various concentrations of curcumin and cell viability was examined using MTT assay, apoptosis was analysed using flow cytometry, reactive oxygen species (ROS) levels using dihydroethidium, LDH release using an LDH cytotoxicity assay, and protein expression using western blot. RESULTS: Curcumin increased the expression of the GSDME N-terminus and proteins involved in pyrolysis, promoted HspG2 cell pyrolysis and increased intracellular ROS levels. Moreover, inhibition of the production of intracellular ROS with n-acetylcysteine (NAC) improved the degree of apoptosis and pyrolysis induced by curcumin. CONCLUSION: Curcumin induces HspG2 cell death by increasing apoptosis and pyroptosis, and ROS play a key role in this process. This study improves our understanding of the potential anti-cancer properties of curcumin in liver cancer.

Picrasma quassioides Extract Elevates the Cervical Cancer Cell Apoptosis Through ROS-Mitochondrial Axis Activated p38 MAPK Signaling Pathway.

BACKGROUND/AIM: Picrasma quassioides (P. quassioides) is used in traditional Asian medicine widely for the treatment of anemopyretic cold, eczema, nausea, loss of appetite, diabetes mellitus, hypertension etc. In this study we aimed to understand the effect of P. quassioides ethanol extract on SiHa cervical cancer cell apoptosis. MATERIALS AND METHODS: The P. quassioides extract-induced apoptosis was analyzed using the MTT assay, fluorescence microscopy, flow cytometry and western blotting. RESULTS: P. quassioides extract induced cellular apoptosis by increasing the accumulation of cellular and mitochondrial reactive oxygen species (ROS) levels and inhibiting ATP synthesis. Pretreatment with N-Acetylcysteine (NAC), a classic antioxidant, decreased the intracellular ROS production and inhibited apoptosis. In addition, the P38 MAPK signaling pathway is a key in the apoptosis of SiHa cells induced by the P. quassioides extract. CONCLUSION: The P. quassioides extract exerts its anti-cancer properties on SiHa cells through ROS-mitochondria axis and P38 MAPK signaling. Our data provide a new insight for P. quassioides as a therapeutic strategy for cervical cancer treatment.

Anti-tumor Properties of Picrasma quassioides Extracts in H-RasG12V Liver Cancer Are Mediated Through ROS-dependent Mitochondrial Dysfunction.

BACKGROUND: Picrasma quassioides (PQ) is a traditional Asian herbal medicine with anti-tumor properties that can inhibit the viability of HepG2 liver cancer cells. H-Ras is often mutated in liver cancer, however, the effect of PQ treatment on H-Ras mutated liver cancer is unclear. This study aimed to investigate the role of PQ on ROS accumulation and mitochondrial dysfunction in H-ras mutated HepG2 (HepG2G12V) cells. MATERIALS AND METHODS: PQ ethanol extract-induced HepG2G12V apoptosis was analyzed by the MTT assay, fluorescence microscopy, flow cytometry and western blotting. RESULTS: PQ treatment affected cell migration and colony formation in HepG2G12V cells. Cleaved-caspase-3, cleaved-caspase-9 and BCL2 associated agonist of cell death (BAD) expression levels were increased, while the levels of B-cell lymphoma-extra large (Bcl-xL) were decreased with PQ treatment. PQ treatment led to a reduction of H-Ras expression levels in liver cancer cells, thus reducing their abnormal proliferation. Furthermore, it led to increased expression levels of Peroxiredoxin VI, which regulates the redox signal in cells. CONCLUSION: Taken together these results provide a new functional significance for the role of PQ in treating HepG2G12V liver cancer.

Peroxiredoxin V Reduces ß-Lapachone-induced Apoptosis of Colon Cancer Cells.

BACKGROUND/AIM: Peroxiredoxin (Prx) V has been known as an antioxidant enzyme which scavenges intracellular reactive oxygen species (ROS). Also, Prx V has been shown to mediate cell apoptosis in various cancers. However, the mechanism of Prx V-induced apoptosis in colon cancer cells remains unknown. Thus, in this study we analyzed the effects of Prx V in ß-lapachone-induced apoptosis in SW480 human colon cancer cells. MATERIALS AND METHODS: ß-lapachone-induced apoptosis was analyzed by the MTT assay, western blotting, fluorescence microscopy, Annexin V staining and flow cytometry. RESULTS: Overexpression of Prx V, significantly decreased ß-lapachone-induced cellular apoptosis and Prx V silencing increased ß-lapachone-induced cellular apoptosis via modulating ROS scavenging activity compared to mock SW480 cells. In addition, to further explore the mechanism of Prx V regulated ß-lapachone-induced SW480 cells apoptosis, the Wnt/ß-catenin signaling was studied. The Wnt/ ß-catenin signaling pathway was found to be induced by ß-lapachone. CONCLUSION: Prx V regulates SW480 cell apoptosis via scavenging ROS cellular levels and mediating the Wnt/ß-catenin signaling pathway, which was induced by ß-lapachone.

[Adsorbing capability of chromium-galvanized waste water by yeast-activated sludge].

The capability of bioadsorption and bioreduction of chromium-galvanized wastewater by Candida lipolytica 1977, Candida utilis 1225, and activated sludge was discussed in this paper. The experimental results showed that the feasible pH range for C. lipolytica 1977 adsorption was wide. The removal and reduction ratios of C. lipolytica 1977 towards chromium-galvanized wastewater were 85.0%, and 100%, when pH was 3.2-6.0, and the concentrations of Cr(total) and Cr6+ were 30.2 mg/L, 27.7 mg/L respectively. The removal ratio increased to 91.1%, when the chromium-galvanized wastewater was treated by two strains together. The aerobic bioadsorption treatment of chromium-galvanized wastewater was investigated. The results demonstrated that this method was the optimal one for the treatment of this kind of wastewater in the study, the removal ratio was 93.8%, when the concentrations of yeast, activated sludge, Cr(total) and Cr6+ were 10 g/L, 5 g/L, 50.3 mg/L and 46.2 mg/L, respectively. The removal ratio increased to 99.5% accordingly, when the activated sludge content was 10 g/L.