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Xu, Rongming, Qinghua Ji, Pin Zhao, Meipeng Jian, Chao Xiang, Chengzhi Hu, Gong Zhang, et al. "Hierarchically porous UiO-66 with tunable mesopores and oxygen vacancies for enhanced arsenic removal." Journal of Materials Chemistry A 8, no. 16 (2020): 7870–79. http://dx.doi.org/10.1039/c9ta13747e.
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Song, Zhao, Shikha Garg, Jinxing Ma, and T. David Waite. "Selective Arsenic Removal from Groundwaters Using Redox-Active Polyvinylferrocene-Functionalized Electrodes: Role of Oxygen." Environmental Science & Technology 54, no. 19 (September 14, 2020): 12081–91. http://dx.doi.org/10.1021/acs.est.0c03007.
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Coles, Cynthia A., and Danial Rohail. "Effect of aeration, iron and arsenic concentrations, and groundwater matrix on arsenic removal using laboratory sand filtration." Environmental Geochemistry and Health 42, no. 11 (July 21, 2020): 4051–64. http://dx.doi.org/10.1007/s10653-020-00671-7.
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Abstract Natural groundwater from the towns of Wabana and Freshwater and treated well water from the town of Wabana in Newfoundland and Labrador, Canada were tested separately and together in sand columns to study the removal of arsenic. The most ideal conditions for arsenic removal appeared to include an arsenic concentration of approximately 35 µg/L and lower, an Fe:As mass ratio in the order of 65 and lower, and aeration of the sand media. Active aeration by pumping air though the filter, passive aeration by scraping off top layers of sand and virtual aeration by diluting the strength of the water being treated, were employed and compared. For tests where groundwater from the towns of Wabana and Freshwater was combined, arsenic removal was optimized and other elements, in addition to iron, were also correlated with effluent arsenic. Further, for these same tests there was a gradual increase in effluent pH that could have been due to oxygen depletion or gradually more reducing conditions in the sand column. Where Ni, Mn and Zn were correlated with effluent arsenic it was concluded that the increase in pH increased heavy metal removal and arsenic release. In the test where the treated Wabana water made up a greater proportion of the mix than the Wabana groundwater, lithium was also correlated with arsenic.
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Azizian-Farsani, Fatemeh, Gholamreza Rafiei, and Mostafa Saadat. "Impact of Sodium Arsenite on Chromosomal Aberrations With Respect to Polymorphisms of Detoxification and DNA Repair Genes." International Journal of Toxicology 33, no. 6 (November 2014): 518–22. http://dx.doi.org/10.1177/1091581814557953.
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Arsenic compounds can increase production of reactive oxygen species. Reactive oxygen species can induce double-strand breaks in DNA, which is a cause of chromosome aberrations (CAs). This study was conducted to determine the association between arsenic exposure and polymorphisms of genes involved in detoxification (glutathione S-transferase T1 [ GSTT1], glutathione S-transferase M1 [ GSTM1], glutathione S-transferase O2 [ GSTO2], catalase [ CAT], and NAD(P)H quinone oxidoreductase1 [ NQO1]) as well as nonhomologous end joining DNA repair genes ( XRCC4, XRCC5, and XRCC6) with induction of chromosomal aberrations. The participants consisted of 123 healthy males who were genotyped using polymerase chain reaction-based methods. Primary cultures of whole blood were treated with sodium arsenite (NaAsO2; iAs(III); at final concentration 1 µmol/L), mitomycin C (at final concentration 60 ηg/mL; as positive control), or untreated. For each culture, mitotic index (MI), chromatid breaks (CBs), CAs, and total percentage of aberrant cells were determined. The levels of CB and percentage of aberrant cells were significantly higher in the TT genotype of CAT (C-262T polymorphism) than the CC genotype. The CB value in samples with GSTM1 active genotype was significantly higher than the null genotype. The MI in samples with TT genotype of NQO1 (C609T polymorphism) was significantly higher than MI in samples having CC and CT genotypes. There was no association between MI, CB, CA, and percentage of aberrant cells and polymorphisms of XRCC4, XRCC5, and XRCC6.
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Brown, Megan, Marcia Bellon, and Christophe Nicot. "Emodin and DHA potently increase arsenic trioxide interferon-α–induced cell death of HTLV-I–transformed cells by generation of reactive oxygen species and inhibition of Akt and AP-1." Blood 109, no. 4 (October 31, 2006): 1653–59. http://dx.doi.org/10.1182/blood-2006-04-015537.
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Abstract Adult T-cell leukemia (ATL) is an aggressive lymphoproliferative disease of poor clinical prognosis associated with infection by the human T-cell leukemia virus type I (HTLV-I). The use of arsenic trioxide (As2O3) has been shown to effectively treat acute promyelocytic leukemia (APL) with greater than 80% of patients achieving complete remission. The combination of arsenic and interferon has also shown promising results in the treatment of ATL. The requirement for slow dosage increases of arsenic and the time required to achieve a pharmacologic active dose in patients is a major obstacle because median survival of patients with ATL is about 6 months. In this study we report a potent synergistic effect of the combination of arsenic trioxide and interferon α (As/IFN-α) with emodin and DHA on cell-cycle arrest and cell death of HTLV-I–infected cells. Importantly, we found that clinically achievable doses of DHA and emodin allowed for reduced arsenic concentrations by 100-fold while still remaining highly toxic to tumor cells. Our data provide a rationale for combined use of As/IFN-α with emodin and DHA in patients with ATL refractory to conventional therapy.
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Ali, Sk Sajed, Nandita Medda, Sangita M. Dutta, Ritesh Patra, and Smarajit Maiti. "Protection against Mitochondrial Oxidative-Stress by Flesh-Extract of Edible Freshwater Snail Bellamya bengalensis Prevents Arsenic Induced DNA and Tissue Damage." Anti-Cancer Agents in Medicinal Chemistry 20, no. 10 (August 20, 2020): 1266–73. http://dx.doi.org/10.2174/1871520620666200410081535.
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Aims: Arsenic has carcinogenic properties because of the formation of Reactive Oxygen Species (ROS). ROS damages different macromolecules, tissues and organs, and severely exhausts cellular antioxidants. Background: Cytosolic and mitochondrial contribution of ROS production by arsenic are not well reported. In regard to the issues of therapy against arsenic or any other toxicity, natural product has gained its popularity due to its less side-effects and non-invasive nature. Objectives: Here, as an ethnomedicine, the flesh-extract (BBE; 100mg/100g bw) of Bellamya bengalensis (an aquatic mollusk) was applied in arsenic intoxicated (0.6 ppm/100g bw/for 28 days alone or in combination with BBE) experimental rats. Our objective was to study the anti-oxidative and anti-apoptotic role of BBE in hepato-gastrointestinal tissue damage by arsenic. Methods: DNA fragmentation assay, catalase activity (gel-zymogram assay) suggests that BBE has a strong protective role against arsenic toxicity, which is decisively demonstrated in hepatic histoarchitecture study by HE (hematoxylin and eosin) staining and by intestinal PAS (Periodic Acid Schiff) staining. Results: Measurement of mitochondrial-membrane-potential by fluorescent microcopy clearly demonstrated less membrane damage and lower release of the redox-active inner-membrane product (cytochrome-C, ubiquinone, etc.) in BBE supplemented group compared to that of the only arsenic fed group. The present study clearly suggests that mitochondrial disintegrity is one of the major causes of ROS mediated tissue damage by arsenic. Conclusions: This study also offers an option for prevention/treatment against arsenic toxicity and its carcinogenicity by widely available low-cost, non-invasive Bellamya extract by protecting cytoskeleton, DNA and mitochondria in the cell.
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Yu, Nan-Hui, Haiping Pei, Yong-Pan Huang, and Yu-Fei Li. "(-)-Epigallocatechin-3-Gallate Inhibits Arsenic-Induced Inflammation and Apoptosis through Suppression of Oxidative Stress in Mice." Cellular Physiology and Biochemistry 41, no. 5 (2017): 1788–800. http://dx.doi.org/10.1159/000471911.
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Background/Aims: Exposure to arsenic in individuals has been found to be associated with various health-related problems including skin lesions, cancer, and cardiovascular and immunological disorders. (-)-Epigallocatechin-3-gallate (EGCG), the main and active polyphenolic catechin present in green tea, has shown potent antioxidant, anti-apoptotic and anti-inflammatory activity in vivo and in vitro. Thus, the present study was conducted to investigate the protective effects of EGCG against arsenic-induced inflammation and immunotoxicity in mice. Methods: Serum IL-1β, IL-6 and TNF-α were determined by ELISA, tissue catalase (CAT), malonyldialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), nitric oxide and caspase 3 by commercial kits, mitochondrial membrane potential with Rh 123, mitochondrial ROS with 2’,7’-dichlorofluorescin diacetate (DCFH-DA), apoptotic and necrotic cells and T-cell phenotyping with Flow cytometry analysis. Results: The results showed that arsenic treatment significantly increased oxidative stress levels (as indicated by catalase, malonyldialdehyde, superoxide dismutase, glutathione and reactive oxygen species), increased levels of inflammatory cytokines and promoted apoptosis. Arsenic exposure increased the relative frequency of the CD8+(Tc) cell subpopulation (from 2.8 to 18.9%) and decreased the frequency of CD4+(Th) cells (from 5.2 to 2.7%). Arsenic exposure also significantly decreased the frequency of T(CD3) (from 32.5% to 19.2%) and B(CD19) cells (from 55.1 to 32.5%). All of these effects induced by NaAsO2 were attenuated by EGCG. Conclusions: The present in vitro findings indicate that EGCG attenuates not only NaAsO2-induced immunosuppression but also inflammation and apoptosis.
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Miller, Wilson H., Izidore S. Lossos, Paul R. Conkling, Carlos Becerra, Martin S. Tallman, Jill Buck, Barbara Wallner, and Jonathan Lewis. "Darinaparsin a Novel Organic Arsenic Molecule Active in Lymphoma: Development of An Oral Form." Blood 114, no. 22 (November 20, 2009): 4759. http://dx.doi.org/10.1182/blood.v114.22.4759.4759.
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Abstract Abstract 4759 Introduction Darinaparsin is an organic arsenic molecule constructed of dimethylated arsenic linked to glutathione (N-[S-(dimethylarsino)-N-L-gamma-glutamyl-L-cysteinyl]-glycine). It has a multifaceted mechanism of action, inducing G2/M cell cycle arrest and apoptosis mediated through disruption of mitochondrial functions, increased reactive oxygen species production, and modulation of signal transduction pathways. In addition, darinaparsin has anti-angiogenic activity. It has significant activity in a broad spectrum of hematologic and solid tumors in preclinical models, including human cell lines resistant to arsenic trioxide. It is active in heavily treated patients with refractory lymphoma when administered IV 300 mg/m2 for 5 days on a 28 day cycle, and is very well tolerated. Preclinically it is orally highly bioavailable. Oral administration may be of importance in potential utility in lymphoma in continuous metronomic dosing. Methods Two Phase I studies of oral darinaparsin are being conducted in patients diagnosed with relapsed or refractory advanced tumors. The first protocol is a Phase I, dose-escalation, oral administration study designed to determine the MTD of darinaparsin capsules. The dosing schedule is a regimen of 2 doses per week for 3 weeks followed by 1 week of rest, starting at 300 mg twice weekly. A second Phase I study, having a similar design and objective, evaluates several dosing regimens, including dosing capsules three times per week increasing dosing frequency to daily dosing for 3 weeks, with 1 week of rest. For each study 28 days constitutes one cycle. Standard methods for evaluation of toxicity, escalation and efficacy are being used. Results These two studies have thus far enrolled 19 and 17 patients, respectively. In total there are 24 male and 12 female patients. The median age is 59 years, with a range from 38 to 82 years. To date, MTD has not been reached in either study. The dose continues to be escalated and is currently at 900mg / day twice weekly in the 1st study, and 300 mg daily every day in the 2nd study. Bioavailability has been very high (>75%). All patients were heavily pretreated and refractory. Of 27 evaluable patients thus far in the two trials, 2 had a partial response and 15 had prolonged stable disease, including lymphoma (NHL), head and neck, colon, and pancreatic cancers. The duration of responses has been 3 – 8 + months. Safety and tolerability has been very good and comparable to that of IV darinaparsin. SAEs were atrial fibrillation and congestive heart failure, each occurring in one patient, and dyspnea, occurring in two patients. No QT prolongation has been observed. Dose escalation continues in both studies and updated results will be presented. Conclusion Darinaparsin is a novel organic arsenic molecule that has demonstrated clinical activity in refractory lymphoma when given IV. When given orally by capsule, the drug is well tolerated and demonstrates early signs of activity. Disclosures: Buck: ZIOPHARM Oncology: Employment. Wallner:ZIOPHARM Oncology: Employment. Lewis:ZIOPHARM Oncology: Employment, Membership on an entity's Board of Directors or advisory committees.
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Ciornea, Elena Todirascu, Gabriela Dumitru, Marius Zaharia, Gabi Drochioiu, and Ion Sandu. "Heavy Metal Pollution Affects the Antioxidant Potential of Rosa canina L. Species." Revista de Chimie 69, no. 2 (March 15, 2018): 449–52. http://dx.doi.org/10.37358/rc.18.2.6125.
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The content of vitamin C, carotenes, polyphenols, total carbohydrates and total soluble proteins was determined, alongside with the activity of the oxidative stress enzymes (superoxide-dismutase, catalase, peroxidase, isocitrat-dehydrogenase, ketoglutarat-dehydrogenase, succinat-dehydrogenase and malat-dehydrogenase) in Rosa canina L. samples collected from the heavy metals and arsenic polluted area around of Tarni�a closed mine, as well as from Sucevita area (as unpolluted site). The results showed an increase in the rose hip richness of nutrients and biological-active compounds, as well as the antioxidant activity of the samples from Tarnita area.We have explained our results taking into consideration the response of rosa plants to the oxidative stress produced by the accumulation of reactive oxygen species generated byexposure to pollutant factors from the contaminated area.
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Soares, Cristina, Paula Paíga, Marta Marques, Tânia Neto, Ana Paula Carvalho, Alexandre Paiva, Pedro Simões, et al. "Multi-Step Subcritical Water Extracts of Fucus vesiculosus L. and Codium tomentosum Stackhouse: Composition, Health-Benefits and Safety." Processes 9, no. 5 (May 19, 2021): 893. http://dx.doi.org/10.3390/pr9050893.
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Mental health and active aging are two of the main concerns in the 21st century. To search for new neuroprotective compounds, extracts of Codium tomentosum Stackhouse and Fucus vesiculosus L. were obtained through multi-step (four step) subcritical water extraction using a temperature gradient. The safety assessment of the extracts was performed by screening pharmaceutical compounds and pesticides by UHPLC-MS/MS, and iodine and arsenic levels by ICP-MS. Although the extracts were free of pharmaceutical compounds and pesticides, the presence of arsenic and high iodine contents were found in the first two extraction steps. Thus, the health-benefits were only evaluated for the fractions obtained in steps 3 and 4 from the extraction process. These fractions were tested against five brain enzymes implicated in Alzheimer’s, Parkinson’s, and major depression etiology as well as against reactive oxygen and nitrogen species, having been observed a strong enzyme inhibition and radical scavenging activities for the step 4 fractions from both seaweed species. Regarding the variation of the chemical composition during the extraction, step 1 fractions were the richest in phenolic compounds. With the increase in temperature, Maillard reaction, caramelization and thermo-oxidation occurred, and the resulting products positively affected the antioxidant capacity and the neuroprotective effects.
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Berenson, J. R., S. Jaganath, D. Reece, R. Boccia, R. Soebel, A. Belch, B. Schwartz, R. P. Gale, and M. Hussein. "ZIO-101 (S-dimethylarsino-glutathione): Phase I/II trials in advanced/progressive multiple myeloma." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 8109. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.8109.
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8109 Background: ZIO-101(S-dimethylarsino-glutathione), a novel organic arsenic, is active against multiple cancers including myeloma in vitro and in animal models. In vitro, it is active at low concentrations in cancers resistant to arsenic trioxide. Anti-cancer activity is multifaceted and is mediated by disrupted mitochondrial function, increased reactive oxygen species (ROS) production, modified signal transduction and anti-angiogenesis. Methods: (1) Phase I/II study to determine maximum tolerated dose (MTD), dose- limiting toxicity (DLT), safety-profile and preliminary efficacy in patients with advanced/progressive myeloma receiving ZIO-101 daily for 5 consecutive d every 4 w; (2) comparison of this schedule at MTD with a schedule of 420 mg/me2/d twice/w for 3 w every 4 w. Results: (1) phase I/ II: 19 patients have been treated so far. Median age is 61 y (range, 41–84 y). Median N prior therapies was 8 (range, 4–10). ZIO-101 was well-tolerated; MTD was 420 mg/me2/d for the 5 d schedule, and DLT was transient confusion /ataxia. No clinically- important biochemical, bone marrow, or cardiac toxicities were seen and there was neither neuropathy nor QTc-prolongation. Pain during peripheral infusion was reported in some patients. Anemia was the only adverse event = grade-3 in 25% of subjects. 6 of 14 evaluable subjects had stable disease (SD) =8 w and 2, SD > 6 mo. Accrual to the phase II portion continues. Conclusions: ZIO-101 was well- tolerated. In the daily for 5 consecutive d every 4 w schedule, the MTD is 420 mg/me2/d and DLT, transient confusion /ataxia. There was SD in 43% of patients with advanced/progressive myeloma, of whom half are beyond 6 months. Accrual into the phase II part of this study continues. No significant financial relationships to disclose.
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Cheng, Xiaodong, Manshouri Taghi, Peng Huang, Mirna Golemovic, Ralph Zingaro, Emil J. Freireich, Michael Andreeff, Hagop M. Kantarjian, and Srdan Verstovsek. "Mechanisms of Increased Reactive Oxygen Species (ROS) Generation Induced by Organic Arsenic Derivative S-Dimethylarsino-Glutathione (SGLU; ZIO-101)." Blood 106, no. 11 (November 16, 2005): 4445. http://dx.doi.org/10.1182/blood.v106.11.4445.4445.
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Abstract ZIO-101 is organic arsenic with similar anti-leukemia activity to arsenic trioxide (ATO) but much less toxicity. Consequently, ZIO-101 can be given at substantially higher doses than ATO and may be active in more diverse cancers than ATO. The precise anti-cancer mechanism of ZIO-101 is unknown: ZIO-101 increases intracellular production of reactive oxygen species (ROS) in dose dependent manner, resulting in apoptosis of leukemic cells. Modifying intracellular ROS levels alters the ability of ZIO-101 to induce apoptosis. We focused on the 2 most important intracellular ROS generators, mitochondria and NADPH oxidase. Cells were treated with ZIO-101 and NADPH oxidase expression levels, membrane translocation and interactions of subunits were studied. Effects of modified NADPH oxidase levels on ZIO-101-induced ROS production were studied (diphenyleneiodonium [DPI], a specific inhibitor of NADPH oxidase, and SiRNA technique were used to inhibit enzyme function, while bryostatin-1, a specific activator of NADPH oxidase, was used to increase enzyme function). Mitochondrial DNA-depleted HL60 Rho-0 cells were also used to evaluate mitochondrial input to ROS-generation. Our data show that ZIO-101 activates NADPH oxidase. A low concentration of ZIO-101 (1uM) requires 14 h to significantly increase intracellular ROS levels and kill leukemic cell. This effect is strongly inhibited by DPI-pretreatment and is also seen in P47-SiRNA transfected HL60 cells. On the other hand, this A higher dose of ZIO-101 (4uM) increases ROS levels more rapidly (2–6 h). This early increase is not inhibited by DPI-pretreatment or SiRNA transfection. A 14 h but not 2–6 h increase in ROS is detectable in Rho-0 HL60 cells. These data indicate dose-dependent mechanisms of ZIO-101 induction of ROS: 1uM ZIO-101 induces NADPH oxidase activity which results in ROS production detectable at 14 h; there is no mitochondrial component; 4uM ZIO-101 disrupts mitochondrial function resulting in an earlier increase in ROS levels and subsequent apoptosis. effect is significantly enhanced in cells that have increased enzyme function. ROS-production in Rho-0 HL60 cells is unaffected by these interventions.
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Mun, Yeung-Chul, Jee-Young Ahn, Eun-Sun Yoo, Jungwon Huh, Kyoung Eun Lee, Eunmi Nam, Soon Nam Lee, and Chu-Myong Seong. "Oxidation Of Peroxiredoxins By Thioredoxin Inactivation Is Mediated In Arsenic Trioxide-Induced Reactive Oxygen Species Formation and Its Cytotoxicity In Acute Promyelocytic Leukemia Cells." Blood 122, no. 21 (November 15, 2013): 3858. http://dx.doi.org/10.1182/blood.v122.21.3858.3858.
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Abstract Backgrounds The Arsenic trioxide (ATO) is an effective cancer therapeutic drug for acute promyelocytic leukemia (APL). ATO exerts its effect mainly raising oxidative stress. However, not only the mechanisms of reactive oxygen species (ROS) generation by ATO but involvement of redox enzymes including peroxiredoxin (PRX) and thioredoxin (TRX) remains elusive. Aim of current study is to elucidate the mechanism of redox enzymes to elevate ROS during ATO-induced apoptosis in APL-derived NB4 cells. Methods NB4 cell line, which is one of the human acute promyelocytic leukemia cell lines, was cultured in RPMI-1640 medium supplemented with 10% FBS in CO2 humidified atmosphere at 37°C. NB4 cells were cultured with 2 μM arsenic trioxide to induce apoptosis for 16-48 hours. Apoptosis was measured by staining with 7-amino-actinomycin D (7-AAD) with flow cytometry. 2, 7-dichlrodihydro-fluorescein-diacetate (H2DCF-DA) and MitoSOX Red were used to detect cellular and mitochondrial ROS. SO2 form for PRX I, PRX II, and PRX III was detected by western blot assay using PRX SO2 form-specific antibody. Monomer/Dimer assay for PRX I, PRX II, PRX III, and TRX I was performed by western blot using non-reducing gel. Results Intracellular ROS of NB4 cells was increased significantly after 16 hour of ATO but decreased after 24 hour of ATO. Mitochondrial ROS of NB4 cells was increased significantly after 39 hour of ATO. Apoptosis of NB4 cell after ATO treatment was increased as time elapsed (24% on 16hr, 26% on 24hr, 48% on 39hr, and 60% on 48hr). Monomer, indicated active and reduced form, of peroxiredoxins was decreased and cysteine sulfinic acid (CP–SO2H) peroxiredoxins, indicated inactive and oxidized peroxiredoxins, was increased in NB4 cells after ATO treatment as time goes by. Similarily, monomer of thioredoxin-1 (active thioredoxin) was decreased and multimer of thioredoxin-1 (inactive thioredoxin) was increased in NB4 cells after ATO treatment as time elapsed. Conclusions Our data showed inactivation of peroxiredoxins by oxidation was developed during ATO-induced ROS generation and APL cell apoptosis. These peroxiredoxins oxidation was probably due to increment of reduced thioredoxin in NB4 cells after ATO treatment. These findings suggest ATO-induced anti-leukemic activity is more likely due to a TRX system-mediated cellular redox changes. Our study may provide the insights for finding novel targets in the development of new therapies, which potentiate ATO-induced apoptosis in APL cells. Disclosures: No relevant conflicts of interest to declare.
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Pang, Su-Yan, Jin Jiang, and Jun Ma. "Oxidation of Sulfoxides and Arsenic(III) in Corrosion of Nanoscale Zero Valent Iron by Oxygen: Evidence against Ferryl Ions (Fe(IV)) as Active Intermediates in Fenton Reaction." Environmental Science & Technology 45, no. 1 (January 2011): 307–12. http://dx.doi.org/10.1021/es102401d.
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Remucal, Christina K., Changha Lee, and David L. Sedlak. "Comment on “Oxidation of Sulfoxides and Arsenic(III) in Corrosion of Nanoscale Zero Valent Iron by Oxygen: Evidence against Ferryl Ions (Fe(IV)) as Active Intermediates in Fenton Reaction”." Environmental Science & Technology 45, no. 7 (April 2011): 3177–78. http://dx.doi.org/10.1021/es104399p.
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Camacho, L. H., D. S. Hong, C. Gutierrez, C. A. Parker, M. A. Purdom, N. M. Tannir, S. Moulder, R. P. Gale, B. Schwartz, and R. Kurzrock. "Organic arsenic in patients (pts) with advanced solid tumors: Phase-1 results of zio-101 (s-dimethylarsino-glutathione)." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 3554. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.3554.
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3554 Background: ZIO-101(S-dimethylarsino-glutathione), a novel organic arsenic, is active against multiple cancers in vitro and in animal models. Anti-cancer activity is multifaceted and is mediated by disrupted mitochondrial function, increased reactive oxygen species (ROS) production, modified signal transduction and anti-angiogenesis. Methods: Phase-1 dose finding study to determine maximum tolerated dose (MTD), dose-limiting toxicity (DLT), pharmacokinetics (PK), and toxicities of ZIO-101 in patients with advanced solid tumors. Results: 34 pts (18 M/16 F) received 78–588 mg/m2/d IV for 5 consecutive days every 4 weeks. Median age was 61 (range, 42–79 y). Median N prior regimens was 3 (1–5). Pts had colorectal (N=17; 12 evaluable), renal (N=4), lung (N=3), melanoma (N=2), pancreas (N=2) and others (N=6). Median N of cycles was 2 (range, 1–12). MTD is 420 mg/m2/d and DLT was transient confusion, and ataxia. Fatigue, nausea and emesis were = grade-2. ZIO-101 was otherwise well-tolerated: There are no hematological toxicities and no QTc- prolongation. Five patients had stable-disease 4–12 mo (colorectal [N=3], renal [N=2],). PK studies at 420 mg/m2/d: tmax = 1 h (SD + 0.9), Cmax = 1.06 μg/L (SD ± 0.07 μg/mL), t1/2 = 17.8 h (SD ± 1.4 h) and AUC0- 8 = 25.9 mg·h/L (SD ± 0.8mg.h/L). 1 pt had complete resolution of a brain metastasis (renal) and 1 patient had a substantial decrease of a liver metastasis (pancreas). Conclusions: ZIO-101 was well tolerated. MTD is 420 mg/m2/d and DLT is transient confusion and ataxia. There was observed clinical benefit in five patients. Expansion cohort is ongoing to further test toxicities and antitumor activity. Phase II studies are ongoing. [Table: see text]
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Pang, Su-Yan, Jin Jiang, and Jun Ma. "Response to Comment on “Oxidation of Sulfoxides and Arsenic(III) in Corrosion of Nanoscale Zero Valent Iron by Oxygen: Evidence against Ferryl Ions (Fe(IV)) as Active Intermediates in Fenton Reaction”." Environmental Science & Technology 45, no. 7 (April 2011): 3179–80. http://dx.doi.org/10.1021/es2004304.
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Douer, Dan, Kristy Watkins, Robert Louie, Ilene Weitz, Ann M. Mohrbacher, Lisa Mark, and Alexandra Levine. "Treatment of Non-APL Acute Myelogenous Leukemia with Intravenous Arsenic Trioxide Plus Ascorbic Acid." Blood 106, no. 11 (November 16, 2005): 4603. http://dx.doi.org/10.1182/blood.v106.11.4603.4603.
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Abstract Introduction: Arsenic trioxide (ATO) is an exceptionally active drug in acute promyelocytic leukemia (APL), inducing complete remissions (CR) in 85% of relapsed patients. ATO also has clinical activity in myelodysplastic syndromes (MDS). In non-APL AML cells lines, ATO induces apoptosis in vitro; however, in a small study of 11 non-APL AML patients, ATO showed no activity (Parmer et al Leuk Res28:090, 2004). ATO-induced apoptosis has been shown to correlate inversely with the level of intracellular reduced glutathione (GSH) via generation of reactive oxygen species; cells with high concentrations of GSH are more resistant to ATO. Ascorbic acid (AA) increases apoptosis and overcomes resistance to ATO in multiple myeloma, non-APL AML and other cell lines by reducing intracellular GSH levels. AA alone has no activity in these cells. We therefore administered ATO plus AA to patients with non-APL AML. Methods: ATO 0.25 mg/kg was administrated intravenously over 1-4 hours with 1 gram of intravenous AA given 30 minutes after ATO daily for five days a week (five days on/2 days off) for five weeks (25 doses=one cycle). These doses were based on a phase I/II trial of ATO + AA in patients with multiple myeloma (Bahlis et al Clin Cancer Res8:3658, 2002)). Responding patients received an additional consolidation cycle of 25 doses followed by maintenance including ATO + AA two weeks of every month for 4 cycles. Patients who failed to respond after two cycles were considered treatment failures. Results: Nine patients aged 36–84 years (median: 66 years) were treated: 5 pts. had refractory AML or relapsed after chemotherapy; 4 elderly pts,. aged 66–84, with antecedent MDS were previously untreated. Activity was seen in 5 (56%) patients, including all 4 of the previously untreated pts: CR in 1 pt. (patient with an early relapse), CRp in 1 pt., decrease in bone marrow blasts to <5% with reduced transfusion requirements in 1 pt, and drop in peripheral blood blasts from 84% and 51% to <5% in 2 patients. Responses were observed after the first treatment cycle. Duration of responses were 6 months in the CR and CRp pts., and 1 week, 2 months. and 4 months in the other responders. Four pts had progressive disease; one patient died on study from progressive disease and infection. Grade 3 /4 toxicity included: infection in 8 pts., and anorexia, sensory neuropathy, elevated bilirubin in 1 pt. each. One responding patient developed shortness of breath with severe hypoxemia, reminiscent of the APL differentiation syndrome, which responded immediately to dexamethasone. Conclusions: ATO + AA has anti-leukemic activity in non-APL AML patients. Despite the high doses of ATO, higher than used in APL and MDS, toxicity was tolerable. This combination could be a less toxic alternative front-line approach to intensive chemotherapy in elderly patients with non-APL AML. Further study of ATO + AA is warranted either alone or in combination with other agents in an attempt to further improve the results.
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Douer, Dan, Kristy Watkins, Robert Louie, Ilene Ceil Weitz, Ann Mohrbacher, Lisa Mark, and Alexandra M. Levine. "Treatment of Non-APL Acute Myelogenous Leukemia with Intravenous Arsenic Trioxide Plus Ascorbic Acid." Blood 108, no. 11 (November 16, 2006): 1959. http://dx.doi.org/10.1182/blood.v108.11.1959.1959.
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Abstract Introduction: Arsenic trioxide (ATO) has demonstrated efficacy in acute promyelocytic leukemia (APL), inducing complete remissions (CR) in 85% of relapsed patients. On the other hand, ATO alone has no activity in non-APL AML. Although this difference could be explained by degradation of the APL specific PML/RAR fusion protein, ATO has shown to be active against APL cells by mechanisms that are independent of this gene rearrangement. ATO-induced apoptosis correlates inversely with intracellular concentrations of reduced glutathione (GSH) via generation of reactive oxygen species (ie, cells with high concentrations of GSH are more resistant to ATO). APL cells were found to have low levels of GSH compared to non-AML cells. Agents that reduce intracellular GSH, such as ascorbic acid (AA), increase ATO-induced apoptosis and can overcome resistance to ATO in non-APL AML cell lines; AA alone has no activity in these cells. Thus, the combination of ATO and AA was evaluated in patients with non-APL AML. Methods: ATO (0.25 mg/kg/d) was administrated intravenously over 1–4 hours with intravenous AA (1g/d, given 30 minutes after ATO) for five days/week (five days on/2 days off) for five weeks (25 doses=one cycle). These doses were based on a phase I/II trial of ATO + AA in patients with multiple myeloma (Behalis et al Clin Cancer Res8:3658, 2002). Responding patients received an additional consolidation cycle of 25 doses followed by maintenance including ATO + AA two weeks of every month for 4 cycles. Patients who failed to respond after two cycles were considered treatment failures. Results: Eleven patients, aged 36–84 years (median: 66 years), were enrolled: 5 had relapsed after chemotherapy; and 6 elderly, aged 66–84, (including 5 with antecedent MDS), were previously untreated. One patient was discontinued prematurely because of QT prolongation. Major response was seen in 3 (27%) pts: CR or CRp in 2 patients and decrease in bone marrow blasts to <5% with reduced transfusion requirements in 1 patient. Three additional patients had a drop in peripheral blood blasts from 85% and 51% to <5%. All responding patients, except for 1, were previously untreated. Responses were observed after the first treatment cycle. Duration of responses were 6 months in the CR and CRp patients, and 1 week, 2 months and 4 months in the other responders. Four pts failed and had progressive disease; one patient died on study from progressive disease and infection. Grade 3/4 toxicity included infection (n=8), and QT (>500 msec), anorexia, fatigue, sensory neuropathy, elevated bilirubin (n=1 each). One responding patient developed shortness of breath with severe hypoxemia, reminiscent of the APL differentiation syndrome, which responded immediately to dexamethasone. Conclusion: ATO + AA can have anti-leukemic activity in poor risk non-APL AML with much less toxicity than chemotherapy, especially in previously untreated patients. Most relapsed patients did not respond to ATO +AA, suggesting that chemotherapy can induce resistance to this combination. Further studies are needed to explore the potential of ATO +AA as a front-line therapy instead of intensive chemotherapy in elderly patients with non-APL AML.
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Alt, H. C. "Electrically Active Oxygen in Gallium Arsenide." Materials Science Forum 83-87 (January 1992): 369–76. http://dx.doi.org/10.4028/www.scientific.net/msf.83-87.369.
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Douer, Dan, Kristy Watkins, Robert Louie, Ilene Weitz, Ann Mohrbacher, and Alexandra M. Levine. "Treatment of Acute Myelogenous Leukemia (non-APL) with Intravenous Trisenox® (Arsenic Trioxide) and Ascorbic Acid: Preliminary Results." Blood 104, no. 11 (November 16, 2004): 1815. http://dx.doi.org/10.1182/blood.v104.11.1815.1815.
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Abstract Introduction: Arsenic trioxide (ATO) is an exceptionally active drug in acute promyelocytic leukemia (APL), inducing complete remissions in 85% of relapsed patients. ATO also has clinical activity in myelodysplastic syndrome (MDS). In non-APL AML cells lines, ATO induces apoptosis in vitro; however, in a small study of 11 non-APL AML patients, ATO showed no activity (Parmer et al Leuk Res28:090, 2004). In some types of cancer cells, ATO-induced apoptosis has been shown to correlate inversely with the level of intracellular reduced glutathione (GSH) via generation of reactive oxygen species; cells with high concentrations of GSH are more resistant to ATO. Ascorbic acid (AA) increases apoptosis and overcomes resistance to ATO in multiple myeloma, non-APL AML and other cell lines by reducing intracellular GSH levels. AA alone has no activity in these cells. We therefore conducted a clinical trial in patients with non-APL AML combining ATO and AA. Methods: ATO at a dose of 0.25 mg/kg is administrated intravenously over 1–3 hour with 1 gram of intravenous AA given within 30 minutes daily for five days a week (five days on/2 days off) for five weeks (25 doses - one cycle). These doses were based on a phase I/II trial of ATO+AA in patients with multiple myeloma (Behalis et al Clin Cancer Res8:3658, 2002)). Responding patients receive an additional consolidation cycle of 25 doses followed by maintenance of two weeks of every month of ATO+ AA for 4 cycles. Patients who fail to respond after two cycles are considered treatment failures. Results: Seven patients have so far enrolled: three (aged 36,52,59) had relapsed after chemotherapy, and four aged 66–84 (median 70), never received chemotherapy. For these untreated patients ATO+AA was given as front line treatment. In three of the four previously untreated patients the number of bone marrow blasts dropped from > 40% to < 5% (2 pts. after 1 cycle; 1 pt. after 2 cycles) At the time of this report only one of the responding patients received more than one cycle and had improvement in the peripheral blood counts. The three patients, who failed chemotherapy, did not respond to ATO+AA (one patient received only one cycle). Despite the high doses of ATO, higher than used in APL and MDS, the combination was very well tolerated with grade 3 toxicity in one patient only (sensory neuropathy). One responding patient developed shortness of breath with severe hypoxemia, reminiscent of the APL differentiation syndrome, which responded immediately to dexamethasone. Conclusion: These preliminary results in patients with non-APL AML suggest that: (1) AA +ATO has anti-leukemia activity in untreated non-APL AML patients with minimal toxicity; (2) more than one cycle is probably needed to achieve a response in the peripheral blood counts; (3) in non-APL AML, ATO can cause the so called “differentiation syndrome” which should be anticipated and treated early. If confirmed in additional patients, ATO+AA might be a less toxic alternative upfront approach to intensive chemotherapy in elderly patients with non-APL AML.
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Alt, H. Ch, Y. V. Gomeniuk, and U. Kretzer. "Charge states and quantitative infrared spectroscopy of electrically active oxygen centers in gallium arsenide." Journal of Applied Physics 101, no. 7 (April 2007): 073516. http://dx.doi.org/10.1063/1.2714001.
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Yamanaka, Kenzo, Akira Hasegawa, Ryoji Sawamura, and Shoji Okada. "Dimethylated arsenics induce DNA strand breaks in lung via the production of active oxygen in mice." Biochemical and Biophysical Research Communications 165, no. 1 (November 1989): 43–50. http://dx.doi.org/10.1016/0006-291x(89)91031-0.
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Тelesh, E. V. "Investigation of the process of reactive ion-beam sputtering of gallium arsenide using optical emission spectroscopy." Doklady BGUIR 19, no. 1 (February 23, 2021): 5–10. http://dx.doi.org/10.35596/1729-7648-2021-19-1-5-10.
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The aim of this work was to study the process of reactive ion-beam sputtering of gallium arsenide using optical emission analysis of plasma in the target region to determine the optimal conditions for the formation of intrinsic GaAs oxides. The ion source was a plasmatron based on an anode layer accelerator (UAS), which generated a stream of accelerated argon and oxygen ions with an energy of 400–1200 eV. The target was made from tellurium doped gallium arsenide. Intense GaI lines (2874.2 Å, 2943.6 Å, 4033.0 Å and 4172.1 Å), atomic argon ArI, argon ions, and also FeI lines were detected in the spectrum upon sputtering of GaAs by Ar+ ions. The appearance of iron lines can be explained by the sputtering of the pole tips of the magnetic system of the ion source. An increase in the accelerating voltage from 1 to 3 kV leads to an increase in the intensity of the peaks of atomic gallium GaI (4172.1 Å) by 2.38 times, the GaI line (4033.0 Å) by 3.25 times, the GaI line (2943.6 Å) 3.4 times, GaI lines (2874.2 Å) 5 times. It was found that an increase in the partial pressure of oxygen leads to a sharp decrease in the peaks of GaI (4033.0 Å) and GaI (4172.1 Å) due to the chemical interaction of gallium and oxygen. Sputtering in pure oxygen reduces the intensity of these peaks by 8 and 5 times, respectively. The intensities of the peaks of atomic gallium GaI (2874.2 Å) and GaI (2943.6 Å) decreased in 2 and 1.78 times, respectively. In the presence of a positive potential on the target, the intensity of all lines of atomic gallium monotonically decreases with increasing potential. In the emission spectrum, lines of atomic oxygen OI (7774.2 Å) and molecular positive ions O+2 (6418.7 Å, 6026.4 Å, 5631.9 Å and 5295.7 Å) were detected. In the presence of a positive potential on the target, a monotonic decrease in the intensity of the above oxygen lines was observed. This indicates an intensification of chemical interaction of oxygen with target elements and, accordingly, a decrease in the free active oxygen particles.
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Sharma, Krishan K., Juan Felipe Rico, Michael W. Becker, Gail J. Roboz, Gabriela Chiosis, and Monica L. Guzman. "HSP70 Inhibitor, YK5, Synergizes with Chemotherapeutic Agents and Prevents Chemoresistance in Acute Myelogenous Leukemia (AML)." Blood 120, no. 21 (November 16, 2012): 2476. http://dx.doi.org/10.1182/blood.v120.21.2476.2476.
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Abstract Abstract 2476 Stress-inducible heat shock protein 70 (HSP70) is a major cytoprotective factor and a molecular chaperone that interacts with HSP90 to form a multi-chaperone complex. Cancer cells are highly dependent on this complex due to their increased demand for protein synthesis. HSP70 overexpression inhibits apoptosis and has been associated with drug resistance and poor prognosis. YK5, a novel inhibitor of tumor-HSP70, has been shown to induce potent cell death in AML blast, progenitor, and stem cell populations with minimal effects in normal hematopoietic cells. Due to the role of HSP70 in drug resistance, we examined the effect of combining YK5 with other chemotherapeutic agents, including arsenic trioxide, cytarabine, suberoylanilide hydroxamic acid (SAHA) and PU-H71, a novel tumor-specific HSP90 inhibitor. We tested the ability of YK5 to synergize with either AsO3, AraC, SAHA, or PU-H71 in primary AML samples. Using multiparameter flow cytometry to measure viability after 48 hours of treatment, we found that combining 1μM YK5 with either 500nM AsO3 or PU-H71 resulted in a significant increase in cell death when compared to either agent alone (n=9, mean viability: 51.8, 67.2, and 13.4% for AsO3, YK5, and AsO3/YK5, respectively, P = 0.0018; mean viability: 57.1 and 20.8% for PU-H71 and PU-H71/YK5, respectively, P = 0.0029). A synergistic relationship between YK5 and both AsO3 and PU-H71 was found in all nine primary samples (combination indexes 0.29 – 0.76 with YK5/AsO3, 0.33 – 0.83 with YK5/PU-H71). In contrast, the combination of YK5 with either AsO3 or PU-H71 in CD34+ cord blood mononuclear cells did not result in a significant increase in cell death when compared to either agent alone (mean viability: 42.4, 72.4, and 37.2% for AsO3, YK5, and AsO3/YK5, respectively; mean viability: 61.1 and 51.1% for PU-H71 and PU-H71/YK5, respectively). YK5 in combination with either AraC or SAHA, however, did not result in a significant increase in cell death when compared to either drug alone, with an additive effect being demonstrated with a 1:1 YK5 to AraC/SAHA drug ratio (Mean CI = 0.9918). To determine the mechanism of the observed synergistic activity, intracellular HSP70 and active caspase-3, a client of HSP70, were measured using flow cytometry. Both AsO3 and PU-H71 significantly increased intracellular HSP70 and caspase-3 (Mean fold change = 18.3, 21.0 of HSP70 and 9.9, 8.3 of Caspase-3 for AsO3 and PU-H71 treatment, respectively), while treatment with AraC or SAHA resulted in no change in HSP70 levels. Furthermore, quantitative PCR revealed that treatment with either AsO3 or PU-H71 strongly upregulated HSPA1A and HSPA6, the main stress-inducible isoforms of HSP70 (Mean fold change = 15.9, 14.1 of HSPA1A, and 20.8, 23.4 of HSPA6 for AsO3 and PU-H71 treatment, respectively). AraC and SAHA had no significant upregulation of these genes. We have previously shown that increased levels of HSPA1A correlate with sensitivity to HSP70 inhibition via YK5. To further explore the mechanism of this observed synergy, flow cytometry was used to measure the levels of reactive oxygen species (ROS). Treatment with AsO3, PU-H71, AraC, or SAHA resulted in a significant increase in ROS (Mean fold change = 2.75, 1.92, 2.89, 1.67, respectively). Quantitative PCR also confirmed the activation of the oxidative stress response by the upregulation of heme oxygenase 1 (HMOX1) by treatment with these drugs (Mean fold change = 10.9, 8.7, 11.2, 7.7, respectively). YK5, however, did not induce ROS or upregulate HMOX1. Interestingly, pretreatment with NAC in primary AML samples (n=4) resulted in no protection from YK5 synergistic effect when combined with either AsO3 or PU-H71. These results suggest that YK5 synergizes with AsO3 and PU-H71 due to the increase in intracellular HSP70 caused by these drugs. This synergy is most likely due to the activation of the heat shock response and independent of the production of ROS due to drug treatment. In summary, we have found that the novel tumor-HSP70 inhibitor YK5 can synergize with AsO3 and PU-H71 in primary human AML, and that the basis of this synergism is due to the increase in intracellular HSP70 caused by these chemotherapeutic agents. HSP70 inhibition represents a novel approach in AML treatment and can be particularly significant to drug-resistant patients when combined with other chemotherapy. Disclosures: Roboz: Astex Pharmaceuticals: Research Funding.
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Li, Rurui, Yuerong Ru, Zhenxing Wang, Xiahong He, Kin-Weng Kong, Tingting Zheng, and Xuechun Zhang. "Phytochemical Composition, Antioxidant Activity, and Enzyme Inhibitory Activities (α-Glucosidase, Xanthine Oxidase, and Acetylcholinesterase) of Musella lasiocarpa." Molecules 26, no. 15 (July 24, 2021): 4472. http://dx.doi.org/10.3390/molecules26154472.
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In this study, we aimed to investigate the chemical components and biological activities of Musella lasiocarpa, a special flower that is edible and has functional properties. The crude methanol extract and its four fractions (petroleum ether, ethyl acetate, n-butanol, and aqueous fractions) were tested for their total antioxidant capacity, followed by their α-glucosidase, acetylcholinesterase, and xanthine oxidase inhibitory activities. Among the samples, the highest total phenolic and total flavonoid contents were found in the ethyl acetate (EtOAc) fraction (224.99 mg GAE/g DE) and crude methanol extract (187.81 mg QE/g DE), respectively. The EtOAc fraction of Musella lasiocarpa exhibited the strongest DPPH· scavenging ability, ABTS·+ scavenging ability, and α-glucosidase inhibitory activity with the IC50 values of 22.17, 12.10, and 125.66 μg/mL, respectively. The EtOAc fraction also showed the strongest ferric reducing antioxidant power (1513.89 mg FeSO4/g DE) and oxygen radical absorbance capacity ability (524.11 mg Trolox/g DE), which were higher than those of the control BHT. In contrast, the aqueous fraction demonstrated the highest acetylcholinesterase inhibitory activity (IC50 = 10.11 μg/mL), and the best xanthine oxidase inhibitory ability (IC50 = 5.23 μg/mL) was observed from the crude methanol extract as compared with allopurinol (24.85 μg/mL). The HPLC-MS/MS and GC-MS analyses further revealed an impressive arsenal of compounds, including phenolic acids, fatty acids, esters, terpenoids, and flavonoids, in the most biologically active EtOAc fraction. Taken together, this is the first report indicating the potential of Musella lasiocarpa as an excellent natural source of antioxidants with possible therapeutic, nutraceutical, and functional food applications.
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Park, Y., M. Skowronski, and T. M. Rosseel. "Alkoxide Doping of GaAs During Organometallic Vapor Phase Epitaxy." MRS Proceedings 282 (1992). http://dx.doi.org/10.1557/proc-282-75.
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ABSTRACTDoping of GaAs with dimethylaluminum methoxide and its effects have been studied during metalorganic vapor phase epitaxy. Oxygen concentration decreases exponentially with increasing growth temperature and the activation energy equal to 1.8 eV.Increase of oxygen content with decrease of V/III ratio indicates that oxygen most likely occupies arsenic site. Photoluminescence intensity was observed to decrease with increasing oxygen contentand three new deep level luminescence peaks appeared at 75, 96, and 160 meV below the band gap. This, together with the fact that as-grown layers are fully depleted, indicates that oxygen is electrically active in OMVPE GaAs and forms deep non-radiative recombinationcenters.
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Jiri, Z., A. Tazvivinga, R. Greenfield, and JHJ Van Vuren. "Oxidative stress biomarkers in Oreochromis niloticus as early warning signals in assessing pollution from acid mine drainage and diffuse sources of pollutants in a subtropical river." Water SA 44, no. 2 April (April 25, 2018). http://dx.doi.org/10.4314/wsa.v44i2.17.
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This study investigated the use of an exotic fish species Oreochromis niloticus as a bio-indicator organism in active biomonitoring of Yellow Jacket and Mazowe rivers, Zimbabwe, receiving acid mine drainage from Iron Duke Mine. The Yellow Jacket River flows through Iron Duke Pyrite Mine while the Mazowe River passes through the Mazowe factory and estate shop that receives runoff from intensive agricultural activities. Active biomonitoring (ABM) exposures were conducted for 6 weeks in effluent-contaminated sections of the rivers during high flow, from February to March 2013. A set of biomarkers of exposure and effect (glutathione S-transferase, catalase and metallothioneins) were selected and their responses determined in O. niloticus liver, gills and muscle. We hypothesized that the increase in activities of GST, CAT and MT in exposed fish, in comparison to control fish, can be used to assess river water quality using O. niloticus. Biomarker expression was measured after 4 and 6 weeks and compared against control fish kept under laboratory conditions without contaminants. Concentrations of zinc, cadmium, chromium, nickel, lead, copper, manganese, arsenic and iron were measured in flowing water, riverbed sediments and muscle tissue of actively biomonitored O. niloticus. Key water quality parameters, including dissolved oxygen and conductivity, clearly showed a pollution gradient from Iron Duke Mine. Expression of CAT and GST was highest in the liver, compared to gills and muscles, after 4 and 6 weeks of exposure, and their expression was lower (p < 0.05) in control fish. The expression of the enzymes was not significantly different after 6 weeks compared to 4 weeks. Increased enzyme expressions at Site 1, which is upstream from Iron Duke Mine, were comparable to enzyme expressions at Sites 3, 4, 5 and 6, which correlated with increased zinc concentrations in the exposed fish muscle tissue. The general order of metal concentrations was sediments > water > fish, except for zinc, which had the highest bioconcentration factors. Using the GST, CAT and MT we concluded that Mazowe and Yellow Jacket rivers are contaminated and that these oxidative stress biomarkers can successfully be used in assessing pollution from point sources such as acid mine drainage, as well as diffuse sources of pollutants such as commercial agriculture.
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Alt, Hans Ch. "Oxygen in Gallium Arsenide." MRS Proceedings 240 (1991). http://dx.doi.org/10.1557/proc-240-871.
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ABSTRACTThe influence of oxygen-related defects on the compensation behavior of semi-insulating gallium arsenide has been studied. Off-center substitutional oxygen (Ga-O-Ga center) forms an electrically active defect with two levels in the fundamental gap. The negative-U ordering of these levels is the origin for very unusual electrical and optical properties. By oxygen implantation and annealing high concentrations of this center are created which are technologically useful to obtain high-resistivity surface layers.
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Varricchi, Gilda, Luca Modestino, Remo Poto, Leonardo Cristinziano, Luca Gentile, Loredana Postiglione, Giuseppe Spadaro, and Maria Rosaria Galdiero. "Neutrophil extracellular traps and neutrophil-derived mediators as possible biomarkers in bronchial asthma." Clinical and Experimental Medicine, August 3, 2021. http://dx.doi.org/10.1007/s10238-021-00750-8.
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AbstractNeutrophils (PMNs) contain and release a powerful arsenal of mediators, including several granular enzymes, reactive oxygen species (ROS) and neutrophil extracellular traps (NETs). Although airway neutrophilia is associated with severity, poor response to glucocorticoids and exacerbations, the pathophysiological role of neutrophils in asthma remains poorly understood. Twenty-four patients with asthma and 22 healthy controls (HCs) were prospectively recruited. Highly purified peripheral blood neutrophils (> 99%) were evaluated for ROS production and activation status upon stimulation with lipopolysaccharide (LPS), N-formylmethionyl-leucyl-phenylalanine (fMLP) and phorbol 12-myristate 13-acetate (PMA). Plasma levels of myeloperoxidase (MPO), CXCL8, matrix metalloproteinase-9 (MMP-9), granulocyte–monocyte colony-stimulating factor (GM-CSF) and vascular endothelial growth factor (VEGF-A) were measured by ELISA. Plasma concentrations of citrullinated histone H3 (CitH3) and circulating free DNA (dsDNA) were evaluated as NET biomarkers. Activated PMNs from asthmatics displayed reduced ROS production and activation status compared to HCs. Plasma levels of MPO, MMP-9 and CXCL8 were increased in asthmatics compared to HCs. CitH3 and dsDNA plasma levels were increased in asthmatics compared to controls and the CitH3 concentrations were inversely correlated to the % decrease in FEV1/FVC in asthmatics. These findings indicate that neutrophils and their mediators could have an active role in asthma pathophysiology.