Journal articles: 'Arsenic cycle'

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Miyashita, Shin-ichi, Shoko Fujiwara, Mikio Tsuzuki, and Toshikazu Kaise. "Cyanobacteria produce arsenosugars." Environmental Chemistry 9, no. 5 (2012): 474. http://dx.doi.org/10.1071/en12061.

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Environmental contextAlthough arsenic is known to accumulate in both marine and freshwater ecosystems, the pathways by which arsenic is accumulated and transferred in freshwater systems are reasonably unknown. This study revealed that freshwater cyanobacteria have the ability to produce arsenosugars from inorganic arsenic compounds. The findings suggest that not only algae, but cyanobacteria, play an important role in the arsenic cycle of aquatic ecosystems. AbstractMetabolic processes of incorporated arsenate in axenic cultures of the freshwater cyanobacteria Synechocystis sp. PCC 6803 and Nostoc (Anabaena) sp. PCC 7120 were examined. Analyses of arsenic compounds in cyanobacterial extracts using a high-performance liquid chromatography–inductively coupled plasma mass spectrometry system showed that both strains have an ability to biotransform arsenate into oxo-arsenosugar-glycerol within 20 min through (1) reduction of incorporated arsenate to arsenite and (2) methylation of produced arsenite to dimethylarsinic acid by methylarsonic acid as a possible intermediate product. In addition, Synechocystis sp. PCC 6803 cells are able to biosynthesise oxo-arsenosugar-phosphate from incorporated arsenate. These findings suggest that arsenosugar formation as well as arsenic methylation in cyanobacteria possibly play a significant role in the global arsenic cycle.

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HANAOKA, Ken'ichi. "Arsenic Cycle in Marine Ecosystmes." Kagaku To Seibutsu 37, no. 10 (1999): 653–59. http://dx.doi.org/10.1271/kagakutoseibutsu1962.37.653.

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Borges Freitas, S. C., D. van Halem, M. M. Rahman, J. Q. J. C. Verberk, A. B. M. Badruzzaman, and W. G. J. van der Meer. "Hand-pump subsurface arsenic removal: the effect of groundwater conditions and intermittent operation." Water Supply 14, no. 1 (September 12, 2013): 119–26. http://dx.doi.org/10.2166/ws.2013.180.

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Hand-pump subsurface arsenic removal (SAR) has been investigated in rural Bangladesh with different groundwater conditions and intermittent operation modes. Multiple injection-abstraction cycles were performed after injection of 1 m3 of aerated water. From these experiments it can be concluded that hand-pump SAR, in the traditional injection-abstraction design, does not provide drinking water below the WHO arsenic guideline of 10 μg/L. Results show that arsenic removal was not enhanced by: (i) injection of O2-rich water, (ii) higher Fe:As ratios in the groundwater, or by (iii) multiple injection-abstraction cycles, i.e. at location 1, the breakthrough occurred at abstraction-injection ratios of Va/Vi = 2, for cycle 23. It is proposed that dissolved organic carbon (DOC), bicarbonate and phosphate have a significant effect on the arsenic adsorption process. However, iron removal was very efficient and abstraction-injection ratios increased within successive cycles, with Va/Vi > 8 for cycle 23. Furthermore, intermittent operation reduced arsenic concentrations after stop and restart, suggesting insufficient contact time between soluble arsenic and oxidized iron surfaces around the tube well.

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Saunders, Jaclyn K., Clara A. Fuchsman, Cedar McKay, and Gabrielle Rocap. "Complete arsenic-based respiratory cycle in the marine microbial communities of pelagic oxygen-deficient zones." Proceedings of the National Academy of Sciences 116, no. 20 (April 29, 2019): 9925–30. http://dx.doi.org/10.1073/pnas.1818349116.

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Microbial capacity to metabolize arsenic is ancient, arising in response to its pervasive presence in the environment, which was largely in the form of As(III) in the early anoxic ocean. Many biological arsenic transformations are aimed at mitigating toxicity; however, some microorganisms can respire compounds of this redox-sensitive element to reap energetic gains. In several modern anoxic marine systems concentrations of As(V) are higher relative to As(III) than what would be expected from the thermodynamic equilibrium, but the mechanism for this discrepancy has remained unknown. Here we present evidence of a complete respiratory arsenic cycle, consisting of dissimilatory As(V) reduction and chemoautotrophic As(III) oxidation, in the pelagic ocean. We identified the presence of genes encoding both subunits of the respiratory arsenite oxidase AioA and the dissimilatory arsenate reductase ArrA in the Eastern Tropical North Pacific (ETNP) oxygen-deficient zone (ODZ). The presence of the dissimilatory arsenate reductase gene arrA was enriched on large particles (>30 um), similar to the forward bacterial dsrA gene of sulfate-reducing bacteria, which is involved in the cryptic cycling of sulfur in ODZs. Arsenic respiratory genes were expressed in metatranscriptomic libraries from the ETNP and the Eastern Tropical South Pacific (ETSP) ODZ, indicating arsenotrophy is a metabolic pathway actively utilized in anoxic marine water columns. Together these results suggest arsenic-based metabolisms support organic matter production and impact nitrogen biogeochemical cycling in modern oceans. In early anoxic oceans, especially during periods of high marine arsenic concentrations, they may have played a much larger role.

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Nadar, S. Venkadesh, Masafumi Yoshinaga, Palani Kandavelu, Banumathi Sankaran, and Barry P. Rosen. "Crystallization and preliminary X-ray crystallographic studies of the ArsI C–As lyase fromThermomonospora curvata." Acta Crystallographica Section F Structural Biology Communications 70, no. 6 (May 10, 2014): 761–64. http://dx.doi.org/10.1107/s2053230x14008814.

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Arsenic is a ubiquitous and carcinogenic environmental element that enters the biosphere primarily from geochemical sources, but also through anthropogenic activities. Microorganisms play an important role in the arsenic biogeochemical cycle by biotransformation of inorganic arsenic into organic arsenicals andvice versa. ArsI is a microbial nonheme ferrous-dependent dioxygenase that transforms toxic methylarsonous acid to the less toxic inorganic arsenite by C–As bond cleavage. An ArsI ortholog from the thermophilic bacteriumThermomonospora curvatawas expressed, purified and crystallized. The crystals diffracted to 1.46 Å resolution and belonged to space groupP43212 or its enantiomerP41212, with unit-cell parametersa=b= 42.2,c= 118.5 Å.

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Rhine, E. Danielle, Elizabeth Garcia-Dominguez, Craig D. Phelps, and L. Y. Young. "Environmental Microbes Can Speciate and Cycle Arsenic." Environmental Science & Technology 39, no. 24 (December 2005): 9569–73. http://dx.doi.org/10.1021/es051047t.

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Han, Yong Hwan, Sung Zoo Kim, Suhn Hee Kim, and Woo Hyun Park. "Arsenic trioxide inhibits growth of As4.1 juxtaglomerular cells via cell cycle arrest and caspase-independent apoptosis." American Journal of Physiology-Renal Physiology 293, no. 2 (August 2007): F511—F520. http://dx.doi.org/10.1152/ajprenal.00385.2006.

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We investigated the in vitro effects of arsenic trioxide on cell growth, cell cycle regulation, and apoptosis in As4.1 juxtaglomerular cells. Arsenic trioxide inhibited the growth of As4.1 cells with an IC50of ∼5 μM. Arsenic trioxide induced S phase arrest of the cell cycle and very efficiently stimulated apoptosis in As4.1 cells, as evidenced by flow cytometric detection of sub-G1DNA content, annexin V binding assay, and 4′-6-diamidino-2-phenylindole staining. This apoptotic process was accompanied by the loss of mitochondrial transmembrane potential (ΔΨm), a decrease in Bcl-2, the activation of caspase-3, and cleavage of poly(ADP-ribose) polymerase. However, all of the caspase inhibitors tested in this experiment failed to rescue As4.1 cells from arsenic trioxide-induced cell death in view of sub-G1cells and annexin V positive-staining cells. However, a caspase-8 inhibitor (Z-IETD-FMK) noticeably decreased the loss of ΔΨmin arsenic trioxide-treated cells. When we examined the changes in reactive oxygen species (ROS), H2O2, or O2•−in arsenic trioxide-treated cells, H2O2was significantly decreased and O2•−was increased. In addition, we detected a decreased GSH content in arsenic trioxide-treated cells. Taken together, we have demonstrated that arsenic trioxide as a ROS generator potently inhibited the growth of As4.1 JG cells through S phase arrest of the cell cycle and caspase-independent apoptosis.

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Dey, Arindam, Sandip Chattopadhyay, Suryashis Jana, Mukul Kumar Giri, Shamima Khatun, Moumita Dash, Hasina Perveen, and Moulima Maity. "Restoration of uterine redox-balance by methanolic extract of Camellia sinensis in arsenicated rats." Acta Biologica Szegediensis 62, no. 1 (August 23, 2018): 7–15. http://dx.doi.org/10.14232/abs.2018.1.7-15.

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Arsenic, an environmental and industrial pollutant causes female reproductive disturbances and female infertility. Several researchers found that the use of Camellia sinensis (CS) (green tea) is effective as an alternative therapeutic strategy in the management of several health ailments. This study explores the role of CS extract against arsenic-induced rat uterine tissue damage. Methanolic extract of CS (10 mg/kg BW) was tested concomitantly in arsenic-treated (10 mg/kg BW) rats for a duration of two-oestrous cycle length (8 days). CS effectively attenuated arsenic-induced antioxidantdepletion and necrosis in uterine tissue. Rats treated with sodium arsenite showed significantlyreduced activities of enzymatic antioxidants like superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) in uterine tissue as evidenced by the results of spectrophotometric and electrozymographic analysis. Co-administration of CS significantly reversed the above oxidative stress markers in uterine tissue along with the histopathological changes in ovarian and uterine tissue. Moreover, an increase in the level of transcription factor NF-κB in the uterine tissue in association with reduced serum levels of vitamin B12 and folic acid were mitigated in arsenic fed rats following CS co-administration.

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Ryan, P. C., F. J. Huertas, L. N. Pincus, and W. Painter. "ARSENIC-BEARING SERPENTINE-GROUP MINERALS: MINERAL SYNTHESIS WITH INSIGHTS FOR THE ARSENIC CYCLE." Clays and Clay Minerals 67, no. 6 (December 2019): 488–506. http://dx.doi.org/10.1007/s42860-019-00040-1.

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Oremland, Ronald S., John F. Stolz, and James T. Hollibaugh. "The microbial arsenic cycle in Mono Lake, California." FEMS Microbiology Ecology 48, no. 1 (April 2004): 15–27. http://dx.doi.org/10.1016/j.femsec.2003.12.016.

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Di, Xuerong, Luke Beesley, Zulin Zhang, Suli Zhi, Yan Jia, and Yongzhen Ding. "Microbial Arsenic Methylation in Soil and Uptake and Metabolism of Methylated Arsenic in Plants: A Review." International Journal of Environmental Research and Public Health 16, no. 24 (December 10, 2019): 5012. http://dx.doi.org/10.3390/ijerph16245012.

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Arsenic (As) poses a risk to the human health in excess exposure and microbes play an important role in the toxicity of As. Arsenic methylation mediated by microbes is a key driver of As toxicity in the environment and this paper reviews the role of microbial arsenic methylation and volatilization in the biogeochemical cycle of arsenic. In specific, little is presently known about the molecular mechanism and gene characterization of arsenic methylation. The uptake of methylated arsenic in plants is influenced by microbial arsenic methylation in soil, thus enhancing the volatilization of methylated arsenic is a potential mitigation point for arsenic mobility and toxicity in the environment. On the other hand, the potential risk of methylated arsenic on organisms is also discussed. And the directions for future research, theoretical reference for the control and remediation of arsenic methylation, are presented.

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Westervelt, Peter, Randy A. Brown, Douglas R. Adkins, Hanna Khoury, Peter Curtin, David Hurd, Selina M. Luger, Margaret K. Ma, Timothy J. Ley, and John F. DiPersio. "Sudden death among patients with acute promyelocytic leukemia treated with arsenic trioxide." Blood 98, no. 2 (July 15, 2001): 266–71. http://dx.doi.org/10.1182/blood.v98.2.266.

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Arsenic trioxide has been shown to be effective in treating acute promyelocytic leukemia (APL), with minimal overall toxicity reported to date. A phase I/II study was initiated in June 1998 using arsenic trioxide for relapsed APL to determine the maximum tolerated or minimal effective dose and to determine the efficacy of treatment at that dose. Ten patients received 1 to 4 monthly cycles of treatment with 0.1 mg/kg per day intravenous arsenic trioxide. Six of 7 patients evaluable for response achieved cytogenetic or molecular complete remission. However, 3 patients died suddenly during the first cycle of treatment. Autopsies obtained on 2 of these failed to identify a cause of sudden death, despite evidence of pulmonary hemorrhage in one. A third patient, for whom an autopsy was not performed, became asystolic and died while on continuous cardiac telemetry. These observations suggest that arsenic trioxide may be significantly or even fatally toxic at doses currently used and that caution is warranted in its use.

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Balares, Kathleen Louise, Joniel Nuevo, Meliton Chiong, Reygie Macasieb, Augustus Resurreccion, and Christian Orozco. "Estimating Energy Consumption and Cost for the Electrocoagulation of Arsenic-laden Water (ECAR) Using Iron Electrodes." E3S Web of Conferences 148 (2020): 01004. http://dx.doi.org/10.1051/e3sconf/202014801004.

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In some areas in Pampanga, arsenic concentration from handpumps reaches up to 300 μg/L, 10 times higher than the safe limit for drinking water. An efficient way of reducing elevated arsenic concentration is through electrocoagulation (EC) process with the use of iron electrodes. However due to several factors, the efficiency of the technique is decreased. This study focuses on determining the energy consumption and cost through time. The cost per cycle was estimated through the power consumption and projecting its growth with time. One 600 L cycle costs around $0.60 to $1.10 which is approximately $0.001 to $0.002 per liter of water. This value increases through each cycle until half of the electrode is consumed (500 cycles) and is to be replaced. The current processing time was set at 30 mins, charge dosage of 150 C/L, applied current of 16.67 mA, and an electrode area of 6.6 cm2. One factor examined which may have caused the increase is the formation of passivation layer on the electrode surface. It was described using linear sweep voltammetry (LSV) and Tafel extrapolation method. The resistance due to charge transfer was determined to be increasing per cycle.

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Tarhini, A. A., J. M. Kirkwood, W. E. Gooding, J. J. Stuckert, and S. S. Agarwala. "A phase II study of arsenic trioxide (ATO) in patients with metastatic melanoma." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 8569. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.8569.

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8569 Background: Arsenic trioxide (ATO) is a promising new agent in the treatment of both solid and hematologic tumors. ATO cytotoxicity and apoptosis induction has been demonstrated in vitro with numerous human cancer cell lines including human melanoma. Methods: We conducted a safety and efficacy single arm study of ATO in patients (18 years or older) with inoperable AJCC stage IV melanoma. One cycle consisted of a loading dose of 0.32 mg/kg/day for 4 days in week 1, followed by 0.25 mg/kg/day twice per week for 6 weeks, followed by 1 week of rest for a total cycle length of 8 weeks when response assessment was performed. Results: A total of 21 patients (5 females and 16 males) were accrued with a median age of 63.8 years (range 32.9 - 81.6). All patients had metastatic melanoma including AJCC stage IV M1a (2), M1b (6) and M1c (13). ECOG performance included 0 (11) and 1 (10). One patient had metastatic choroidal melanoma and 20 had cutaneous melanoma. Twenty patients had received prior therapy including chemotherapy (17), immunotherapy (11) and radiation (3). Six patients completed 1 cycle, seven 2 cycles, one 3 cycles, one 4 cycles and two 5 cycles of ATO. Four patients did not complete the first cycle and are not evaluable for response. Possible treatment related Grade 3/4 toxicities included one case of idiopathic thrombocytopenic purpura and one case of elevated LDH. Among 17 evaluable patients, 1 (6%) had partial response lasting 7 months, 8 (47%) had disease stabilization after 1 cycle, but all eventually progressed. A total of 19 patients have died and 2 are alive at a median follow up of 17.5 weeks. Median time to progression is 14 weeks, 95% CI (9, 38) and median survival is 52.9 weeks, 95% CI (14.4, 66.1). Conclusions: ATO as a single agent is well tolerated with modest activity in metastatic melanoma that may be enhanced in combination with other agents that induce apoptosis. No significant financial relationships to disclose.

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Peltekov, A. B., B. S. Boyanov, and T. S. Markova. "Behavior of arsenic in hydrometallurgical zinc production and environmental impact." Polish Journal of Chemical Technology 16, no. 4 (December 1, 2014): 80–86. http://dx.doi.org/10.2478/pjct-2014-0074.

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Abstract The presence of arsenic in zinc sulphide concentrates is particularly harmful, because it creates problems in zinc electrolysis. The main source of arsenic in non-ferrous metallurgy is arsenopyrite (FeAsS). In oxidative roasting of zinc concentrates, FeAsS oxidizes to arsenic oxides (As2O3, As2O5). In this connection a natural FeAsS was examined, and also the distribution of arsenic in the products of the roasting process, the cycle of sulphuric acid obtaining and the leaching of zinc calcine were studied. The arsenic contamination of soils in the vicinity of nonferrous metals smelter KCM SA, Plovdiv, Bulgaria as a result of zinc and lead productions has been studied.

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Riedel, Gerhardt F. "The Annual Cycle of Arsenic in a Temperate Estuary." Estuaries 16, no. 3 (September 1993): 533. http://dx.doi.org/10.2307/1352600.

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Santosa, Sri Juari, Satoshi Wada, and Shigeru Tanaka. "Distribution and cycle of arsenic compounds in the ocean." Applied Organometallic Chemistry 8, no. 3 (May 1994): 273–83. http://dx.doi.org/10.1002/aoc.590080319.

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Kahl, Brad S., Harish G. Ahuja, Federico A. Sanchez, Gilberto A. Rodrigues, Peter M. Voorhees, Emily A. Stevens, Jamie Smith, Nancy Turman, KyungMann Kim, and Howard H. Bailey. "Phase II Study of Arsenic Trioxide Plus Ascorbic Acid for Relapsed and Refractory Lymphoid Malignancies: A Wisconsin Oncology Network Study." Blood 104, no. 11 (November 16, 2004): 4582. http://dx.doi.org/10.1182/blood.v104.11.4582.4582.

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Abstract Introduction: Arsenic trioxide (AT) has impressive single agent activity in relapsed acute promyelocytic leukemia. It also has activity in myelodysplastic syndromes and multiple myeloma. In vitro data has suggested increased cytotoxicity when combined with agents that deplete intracellular glutathione, forming the rationale for combination studies. Ascorbic acid (AA) can deplete intracellular glutathione and may potentiate the cytotoxicity of AT. Upon this basis, we initiated a phase II study of arsenic trioxide plus ascorbic acid for relapsed/refracory lymphoid malignancies. Arsenic trioxide was administered at a dose of 0.25 mg/kg IV over one hour M-F for one week and then 2X/week for 5 weeks. Each arsenic infusion was followed by an infusion of 1000 mg ascorbic acid over 15 minutes. Each 6-week cycle was followed by a two-week rest period before repeating the cycle. Treatment was continued until best response plus two cycles or progressive disease. Patient characteristics: Median age 70.5 (37–88). Gender 10M, 6F. Histologies CLL/SLL (4), Follicular (3), Mantle Cell (3), DLBCL (2), Burkitt (2), Marginal Zone (1), Hairy Cell (1). Median # Prior therapies 4 (2–13). Refractory to prior treatment 13/16. Median ECOG PS 1 (0–2). B symptoms 3/16. Elevated LDH 8/16. Elevated B2M 13/16. Results: Median number of completed cycles 1 (0–4). Eight patients did not complete cycle #1, six due to progressive disease (PD) and 2 due to toxicity. Of the 2 patients coming off for toxicity, one patient with known coronary artery disease suffered a myocardial infarction on the 4th day of treatment and expired from congestive heart failure and the other experienced repeated grade 4 hyperglycemia. Six patients completed one cycle of therapy and were removed for PD. One patient completed 3 cycles of therapy before experiencing PD. One patient with mantle cell lymphoma received 4 cycles of therapy and achieved a CRu. The overall response rate was 6% (1/16). The responding patient’s treatment was stopped after 4 cycles for MD/patient preference and she experienced PD 5 months after completion of therapy. Grade 3 toxicities included thrombocytopenia (2 patients), anemia (3), neutropenia (1), stomatitis (1), anorexia (1), and elevated LFTs (1). Grade 4 toxicities included neutropenia (2) and hyperglycemia (1). Conclusions: AT plus AA in this dosing schedule had modest toxicity but limited antitumor activity. The data should be interpreted in the context of our heavily treated, essentially refractory patient population. Our trial had a two-stage design, and was closed due to lack of activity at the first stage analysis. Other doses and schedules may prove to be more efficacious.

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Nuntharatanapong, Nopparat, Kai Chen, Palarp Sinhaseni, and John F. Keaney. "EGF receptor-dependent JNK activation is involved in arsenite-induced p21Cip1/Waf1 upregulation and endothelial apoptosis." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 1 (July 2005): H99—H107. http://dx.doi.org/10.1152/ajpheart.00901.2004.

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Arsenic exposure is associated with an increased risk of atherosclerosis and vascular diseases. Although endothelial cells have long been considered to be the primary targets of arsenic toxicity, the underlying molecular mechanism remains largely unknown. In this study, we sought to explore the signaling pathway triggered by sodium arsenite and its implication for endothelial phenotype. We found that sodium arsenite produced time- and dose-dependent decreases in human umbilical vein endothelial cell viability. This effect correlated with the induction of p21Cip1/Waf1 (up to 10-fold), a regulatory protein of cell cycle and apoptosis. We also found that arsenite-stimulated EGF (ErbB1) and ErbB2 receptor transactivation, manifest as receptor tyrosine phosphorylation, appeared to be a proximal signaling event leading to p21Cip1/Waf1 induction, because both pharmacological inhibitors and knockdown of receptors by RNA interference blocked arsenite-induced p21Cip1/Waf1 upregulation. Arsenite-induced activation of JNK and p38 MAPK was distinct, with only JNK as a downstream target of the EGF receptor. Moreover, inhibition of JNK with SP-600125 or dominant negative MKK7 inhibited only p21Cip1/Waf1 induction, whereas the p38 MAPK inhibitor SB-203580 or dominant negative MKK4 inhibited both p21Cip1/Waf1 and p53 induction. Functionally, inhibition of p21Cip1/Waf1 induction prevented endothelial apoptosis due to arsenite treatment. Insofar as endothelial dysfunction promotes vascular disease, these data provide a mechanism for the increased incidence of cardiovascular disease due to arsenite exposure.

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Zeng, Xian-Chun, Guoji E, Jianing Wang, Nian Wang, Xiaoming Chen, Yao Mu, Hao Li, Ye Yang, Yichen Liu, and Yanxin Wang. "Functions and Unique Diversity of Genes and Microorganisms Involved in Arsenite Oxidation from the Tailings of a Realgar Mine." Applied and Environmental Microbiology 82, no. 24 (September 23, 2016): 7019–29. http://dx.doi.org/10.1128/aem.02190-16.

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ABSTRACTThe tailings of the Shimen realgar mine have unique geochemical features. Arsenite oxidation is one of the major biogeochemical processes that occurs in the tailings. However, little is known about the functional and molecular aspects of the microbial community involved in arsenite oxidation. Here, we fully explored the functional and molecular features of the microbial communities from the tailings of the Shimen realgar mine. We collected six samples of tailings from sites A, B, C, D, E, and F. Microcosm assays indicated that all of the six sites contain both chemoautotrophic and heterotrophic arsenite-oxidizing microorganisms; their activities differed considerably from each other. The microbial arsenite-oxidizing activities show a positive correlation with soluble arsenic concentrations. The microbial communities of the six sites contain 40 phyla of bacteria and 2 phyla of archaea that show extremely high diversity. Soluble arsenic, sulfate, pH, and total organic carbon (TOC) are the key environmental factors that shape the microbial communities. We further identified 114 unique arsenite oxidase genes from the samples; all of them code for new or new-type arsenite oxidases. We also isolated 10 novel arsenite oxidizers from the samples, of which 4 are chemoautotrophic and 6 are heterotrophic. These data highlight the unique diversities of the arsenite-oxidizing microorganisms and their oxidase genes from the tailings of the Shimen realgar mine. To the best of our knowledge, this is the first report describing the functional and molecular features of microbial communities from the tailings of a realgar mine.IMPORTANCEThis study focused on the functional and molecular characterizations of microbial communities from the tailings of the Shimen realgar mine. We fully explored, for the first time, the arsenite-oxidizing activities and the functional gene diversities of microorganisms from the tailings, as well as the correlation of the microbial activities/diversities with environmental factors. The findings of this study help us to better understand the diversities of the arsenite-oxidizing bacteria and the geochemical cycle of arsenic in the tailings of the Shimen realgar mine and gain insights into the microbial mechanisms by which the secondary minerals of the tailings were formed. This work also offers a set of unique arsenite-oxidizing bacteria for basic research of the molecular regulation of arsenite oxidation in bacterial cells and for the environmentally friendly bioremediation of arsenic-contaminated groundwater.

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Jones, C. J., D. Laky, I. Galambos, C. Avendano, and V. L. Colvin. "Life cycle analysis of two Hungarian drinking water arsenic removal technologies." Water Supply 14, no. 1 (September 12, 2013): 48–60. http://dx.doi.org/10.2166/ws.2013.165.

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Determining a technology's merit as a solution to Hungarian drinking water arsenic contamination goes beyond technical concerns: environmental and economic aspects also play very important roles. In an effort to address the current arsenic drinking water requirements in Hungary, life cycle analysis (LCA) methodology was applied on two example arsenic removal technologies, coagulation-filtration and adsorption, from cradle to grave. A distribution of 500 m3/day was assumed, along with a range of possible operation boundary conditions modelled solely for As treatment. Nine out of 10 considered impact categories tended to favour coagulation-filtration, however realistic variations in water chemistry and product characteristics led to some overlap of their environmental impact. Unlike other studies on water systems, electricity did not have a large direct impact; this was due to the focussed nature of this study on individual treatment technologies rather than an entire water supply system. Regeneration of the adsorption technology filter material was also observed to require nearly the same mass of materials for one regeneration as what was needed to support the coagulation-filtration technology for an entire year. Hazardous waste was surprisingly not reduced for adsorption compared to coagulation-filtration due to prefiltration requirements and an extra regeneration, even though adsorption shifts some of the environmental burden to the production phase. Additionally, cost analysis observes that coagulation-filtration is the cheaper of the two technologies; its highest cost is that of waste disposal, while the highest single expense modelled is that of the adsorption media cost.

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Liang, Mengyu, Huaming Guo, and Wei Xiu. "Mechanisms of arsenite oxidation and arsenate adsorption by a poorly crystalline manganese oxide in the presence of low molecular weight organic acids." E3S Web of Conferences 98 (2019): 04009. http://dx.doi.org/10.1051/e3sconf/20199804009.

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Manganese oxides are considered as one of the effective oxides capable of oxidizing arsenite and reduce the toxicity of arsenic. Since low molecular weight organic acids (LMWOAs) commonly found in nature can act as reducing and chelating agents for manganese oxides, it is particularly important to investigate how these organic acids with different numbers of carboxyl groups like citrate and EDTA affect oxidation and adsorption of arsenic by manganese oxides. In this study, low As(V) adsorption on manganese oxide is slightly enhanced by citrate and EDTA, which results from the increase in active sites via reduction of manganese oxide by LMWOAs. However, citrate and EDTA have different effects on the oxidation of As(III). MnIII/II citrate autocatalytic cycle as a manganese-based redox system decreases As(III) oxidation rate, but EDTA does not yield autocatalysis, which slightly increases the oxidation rate of As(III). Reduction of manganese oxide by EDTA and chelation between Mn(II) and EDTA lead to exposure of more active sites. Our research highlights the different effects of low molecular weight organic acids on the reactions between arsenic and manganese oxide.

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Douer, Dan, Laleh Ramezani, Kristy Watkins, Robert Louie, and Martin S. Tallman. "Durable Molecular Remission in Two Acute Promyelocytic Leukemia (APL) Patients Treated with Arsenic Trioxide at First Molecular Relapse." Blood 106, no. 11 (November 16, 2005): 1847. http://dx.doi.org/10.1182/blood.v106.11.1847.1847.

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Abstract Background: The recurrent detection of the PML- RARα transcripts in APL patients in complete remission (CR) is predictive of clinical relapse. Intervention at the time of molecular relapse rather than at the time of overt clinical relapse may minimize the risks associated with the disease as well as treatment-related complications. Previous studies have shown that patients treated at molecular relapse had improved overall survival compared to patients treated at clinical relapse; however, the optimal approach to the treatment of molecular relapse has not yet been established. Arsenic trioxide is active as a single agent in APL patients who developed overt clinical relapse after treatment with ATRA and anthracycline chemotherapy. We evaluated the use of single agent arsenic trioxide in APL patients who are still in first hematological CR but have become RT-PCR positive. Methods: So far, 2 patients were studied, both females with the long form of RAR RARα (bcr1), aged 29 and 39 years. These patients had normal bone marrow morphology but were found to be RT-PCR positive twice in an interval of at least 2 months, while in first CR at 12 and 36 months, respectively. Arsenic trioxide, 0.15 mg/kg/dose, was administered intravenously for 5 days per week for 5 weeks (total of 25 doses) with a 3 to 6 week rest period between cycles up to a maximum of 4 cycles. Results: Both patients became PCR negative after the first cycle of arsenic trioxide. One patient completed four cycles of therapy. The second patient had a history of diabetes mellitus, received only 20 doses of the first cycle and was removed from the study because of grade III sensory neurotoxicity. The only other side effects were grade II headache in both patients and self-limited grade III liver toxicity in one patient. Both patients remain RT-PCR negative at 30 and 28 months after enrollment, respectively, without further therapy. Conclusions: Without treatment, these patients could be expected to have developed a clinical relapse within 4–10 months. Arsenic trioxide induced a durable second molecular relapse, extending disease-free survival and obviating the need for more intensive treatment, such as chemotherapy and stem cell transplantation.

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Mestrot, Adrien, Britta Planer-Friedrich, and Jörg Feldmann. "Biovolatilisation: a poorly studied pathway of the arsenic biogeochemical cycle." Environmental Science: Processes & Impacts 15, no. 9 (2013): 1639. http://dx.doi.org/10.1039/c3em00105a.

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Oremland, R. S. "A Microbial Arsenic Cycle in a Salt-Saturated, Extreme Environment." Science 308, no. 5726 (May 27, 2005): 1305–8. http://dx.doi.org/10.1126/science.1110832.

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Lai, Vivian W. M., Katerina Kanaki, Spiros A. Pergantis, William R. Cullen, and Kenneth J. Reimer. "Arsenic speciation in freshwater snails and its life cycle variation." J. Environ. Monit. 14, no. 3 (2012): 743–51. http://dx.doi.org/10.1039/c2em10764c.

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Barrett, Alison K., and Seth M. Rubin. "Heavy metal in cancer: The cell cycle jams with arsenic." Cell Cycle 16, no. 18 (September 1, 2017): 1641–42. http://dx.doi.org/10.1080/15384101.2017.1360653.

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Welch, John S., Jeffery Klco, Feng Gao, Anjum Hassan, and Ravi Vij. "A Phase I Dose-Escalation Study of Combination Decitabine, Arsenic Trioxide and Ascorbic Acid In Patients with MDS and AML." Blood 116, no. 21 (November 19, 2010): 2148. http://dx.doi.org/10.1182/blood.v116.21.2148.2148.

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Abstract Abstract 2148 Introduction: Myelodysplastic syndrome (MDS) and Acute Myeloid Leukemia (AML) are hematological disorders that exist on a spectrum of ineffective and malignant hematopoiesis. Hypomethylating agents have been recently shown to result in clinical response and improved survival in patients with either disease, although only in a minority of patients. Arsenic trioxide too has shown limited single agent activity in patients with MDS and AML, and ascorbic acid improves response to arsenic trioxide in patients with multiple myeloma. We therefore sought to assess the tolerability of combination decitabine, arsenic and ascorbic acid in patients with MDS and AML. Study: The primary object of this single institution, dose-escalation study was to establish the maximum tolerated dose and dose-limiting toxicities during four cycles of therapy. Arsenic trioxide was administered in three dose cohorts of 3–6 patients each: 0.1 mg/kg, 0.2 mg/kg, and 0.3 mg/kg IV on days 1–5 followed by weekly administration for 15 weeks. All patients received decitabine 20 mg/m2 IV on days 1–5 every 28 days and ascorbic acid 1000 mg IV following every administration of arsenic trioxide. Secondary objectives were to establish overall response rates and effect of therapy on bone marrow angiogenesis. Results: Thirteen patients were enrolled in three dose cohorts [9 men, 4 women; median age: 67 (range 24 – 77); 5 MDS, 7 AML; ECOG 0 (46%), 1 (38%), 2 (15%)]. Most patients were transfusion dependent [RBC dependent: MDS 4/5, AML 4/7; platelet dependent: MDS 2/5, AML 4/7]. Most patients had received prior therapy [MDS 1/5; AML 7/7]. Ten patients received at least 2 cycles with four patients completing four cycles. Dose limiting toxicities were pneumonia/infection, which occurred in the third dosing cohort. Other grade 3–4 toxicities occurring during 4 cycles of treatment were: infection (46%), hypotension (15%), hypoxia/pneumonia (20%), anemia (53%), neutropenia (38%), QTc prolongation (15% - all asymptomatic), pericardial effusion (8%), pleural effusion (8%), hyperglycemia (20%), hypokalemia (8%). According to IWG response criteria, 2/5 MDS patients achieved stable disease, 2/5 developed progressive disease, and 1/5 withdrew prior to reevaluation. Similarly, 3/7 AML patients achieved stable disease, 2/7 progressive disease, and 2/7 died without repeat bone marrow evaluation. No transfusion dependent patients achieved transfusion independence. The median overall survival of these cohorts was 207 days and four patients remain alive with a median follow-up of 490 days. We did not observe a correlation between dosing cohort and response or survival. Because arsenic trioxide has been proposed to inhibit angiogenesis, we assessed bone marrow microvessel density (MVD) using CD34 immunohistochemistry by two binded, independent reviewers. Paired bone marrow samples from eight patients surprisingly revealed an increase in the number of vessels per high powered field during therapy [pre-treatment: (ave 10.3, stdev 5.2); after cycle 2: (ave 18.0, stdev 7.0, p = 0.06); after cycle 4: (ave 17.1, stdev 3.2, p = 0.05)]. Increased MVD occurred independent of response, disease or bone marrow cellularity. Conclusions: This study demonstrates that decitabine can be safely combined with arsenic trioxide and ascorbic acid in a heavily pre-treated population of MDS and AML patients. Our maximum tolerated dose of arsenic was observed in cohort 2: 0.2 mg/kg. Combination therapy resulted in increased bone marrow microvessel density, independent of response and bone marrow cellularity. Phase 2 studies will be required to assess the efficacy of combination therapy. Disclosures: Off Label Use: Decitabine, Arsenic and Ascorbic acid for the treatment of AML. Vij: Eisai: Speakers Bureau; Cephalon: Speakers Bureau.

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Nabiyeva, A. A., N. A. Kulenova, and S. V. Mamyachenkov. "Studying Kinetics of Arsenic Recovery from Copper Dross by Alkaline Sulfide Leaching." Materials Science Forum 946 (February 2019): 547–51. http://dx.doi.org/10.4028/www.scientific.net/msf.946.547.

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Copper dross are produced by rough decopperizing of blast furnace lead bullion. During liquation separation of copper dross from lead bullion most of arsenic and copper are concentrated in copper dross, arsenic content is approximately 4% As. Currently the processes for arsenic recovery from copper dross are understudied. In this work the focus is given to studying kinetics of the process for recovering arsenic from copper dross by alkaline-sulfide leaching. Alkaline sulfide leaching allows carrying out selective removal of arsenic into solution, keeping at this non-ferrous and precious metals in leaching residue. The studied method of alkaline sulfide leaching of copper dross provides backgrounds for developing technology that would allow processing of copper dross with selective arsenic removal from lead production cycle. By minimizing circulation of this harmful impurity in lead production it is possible to lessen destructive effect of its aggressive compounds on smelting-units refractory. Kinetics of alkaline sulfide leaching of copper dross was understudied up to date. This work is an attempt to fill the gap.

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Zajáros, Anett, Klára Szita, Károly Matolcsy, and Dániel Horváth. "Life Cycle Sustainability Assessment of DMSO Solvent Recovery from Hazardous Waste Water." Periodica Polytechnica Chemical Engineering 62, no. 3 (November 13, 2017): 305–9. http://dx.doi.org/10.3311/ppch.11097.

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The protection of continuous drinking water supply is really important all over the world, also in Hungary. Many kinds of hazardous chemicals could pollute the natural water resources, arsenic is one of the most occurring pollutant in Hungary. Recently, an ethylene-vinyl alcohol copolymer based arsenic removal adsorbent has been developed. During the manufacturing process hazardous waste water is produced, which is burned in the incineration plant, so this open production process needs fresh solvent every time. However, if the different fraction of the waste water is separated by distillation both the volume of the hazardous waste water can be reduced extremely and the recovered solvent and water can be reused in the manufacturing process. Beside analytical measurements Life Cycle Sustainability Assessment (LCSA) was prepared to identify and compare the environmental, economic and social effects of the current technology and the new one. The results proved that the technology closed by distillation is better than the current open one in each aspect of LCSA.

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Petrusevski, B., W. van der Meer, J. Baker, F. Kruis, S. K. Sharma, and J. C. Schippers. "Innovative approach for treatment of arsenic contaminated groundwater in Central Europe." Water Supply 7, no. 3 (November 1, 2007): 131–38. http://dx.doi.org/10.2166/ws.2007.075.

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Long-term exposure to low arsenic concentrations in drinking water causes different diseases including cancer. Hundreds of millions of people worldwide are exposed to arsenic in drinking water. Within Europe, Hungary, Serbia and Croatia are likely most affected. Elevated arsenic concentration has been found in several wells used by the Water Supply Company in Makó, Hungary. Groundwater in southern Hungary typically contains also ammonia, methane, some iron and manganese. Situation is very similar in several other surrounding countries. There are intensive efforts to find affordable approach for treatment of such complex arsenic contaminated groundwater. UNESCO-IHE has been developing an innovative arsenic removal technology (IHE ADART), based on adsorption on iron oxide coated sand (IOCS) and an in-situ regeneration of exhausted adsorbent. The paper presents results from field-testing of the IHE-ADART technology in Southern Hungary. Two pilot plants have been operated at several arsenic-contaminated wells with arsenic concentrations from 20 to 260 μg/l. Very consistent arsenic removal below 10 μg/l was achieved at all testing wells and throughout the 18 months of continuous testing. In addition methane, ammonia, iron and manganese were removed highly effectively. Life cycle cost analysis showed that overall treatment costs would be below 0.10 Euro/m3.

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Feseke, SK, J. St-Laurent, E. Anassour-Sidi, P. Ayotte, M. Bouchard, and P. Levallois. "Arsenic exposure and type 2 diabetes: results from the 2007–2009 Canadian Health Measures Survey." Health Promotion and Chronic Disease Prevention in Canada 35, no. 4 (June 2015): 63–72. http://dx.doi.org/10.24095/hpcdp.35.4.01.

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Introduction Inorganic arsenic and its metabolites are considered dangerous to human health. Although several studies have reported associations between low-level arsenic exposure and diabetes mellitus in the United States and Mexico, this association has not been studied in the Canadian population. We evaluated the association between arsenic exposure, as measured by total arsenic concentration in urine, and the prevalence of type 2 diabetes (T2D) in 3151 adult participants in Cycle 1 (2007–2009) of the Canadian Health Measures Survey (CHMS). Methods All participants were tested to determine blood glucose and glycated hemoglobin. Urine analysis was also performed to measure total arsenic. In addition, participants answered a detailed questionnaire about their lifestyle and medical history. We assessed the association between urinary arsenic levels and T2D and prediabetes using multivariate logistic regression while adjusting for potential confounders. Results Total urinary arsenic concentration was positively associated with the prevalence of T2D and prediabetes: adjusted odds ratios were 1.81 (95% CI: 1.12–2.95) and 2.04 (95% CI: 1.03–4.05), respectively, when comparing the highest (fourth) urinary arsenic concentration quartile with the lowest (first) quartile. Total urinary arsenic was also associated with glycated hemoglobin levels in people with untreated diabetes. Conclusion We found significant associations between arsenic exposure and the prevalence of T2D and prediabetes in the Canadian population. Causal inference is limited due to the cross-sectional design of the study and the absence of long-term exposure assessment.

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Hung, C. Y., J. S. Harris, A. F. Marshall, and R. A. Kiehl. "Annealing cycle dependence of preferential arsenic precipitation in AlGaAs/GaAs layers." Applied Physics Letters 73, no. 3 (July 20, 1998): 330–32. http://dx.doi.org/10.1063/1.121824.

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Lièvremont, Didier, Philippe N. Bertin, and Marie-Claire Lett. "Arsenic in contaminated waters: Biogeochemical cycle, microbial metabolism and biotreatment processes." Biochimie 91, no. 10 (October 2009): 1229–37. http://dx.doi.org/10.1016/j.biochi.2009.06.016.

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van Halem, D., S. G. J. Heijman, R. Johnston, I. M. Huq, S. K. Ghosh, J. Q. J. C. Verberk, G. L. Amy, and J. C. van Dijk. "Subsurface iron and arsenic removal: low-cost technology for community-based water supply in Bangladesh." Water Science and Technology 62, no. 11 (December 1, 2010): 2702–9. http://dx.doi.org/10.2166/wst.2010.463.

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The principle of subsurface or in situ iron and arsenic removal is that aerated water is periodically injected into an anoxic aquifer through a tube well, displacing groundwater containing Fe(II). An oxidation zone is created around the tube well where Fe(II) is oxidised. The freshly formed iron hydroxide surfaces provide new sorption sites for soluble Fe(II) and arsenic. The system's efficiency is determined based on the ratio between abstracted volume with reduced iron/arsenic concentrations (V) and the injected volume (Vi). In the field study presented in this paper, the small-scale application of this technology was investigated in rural Bangladesh. It was found that at small injection volumes (<1 m3) iron removal was successful and became more effective with every successive cycle. For arsenic, however, the system did not prove to be very effective yet. Arsenic retardation was only limited and breakthrough of 10 μg/L (WHO guideline) was observed before V/Vi=1, which corresponds to arrival of groundwater at the well. Possible explanations for insufficient arsenic adsorption are the short contact times within the oxidation zone, and the presence of competing anions, like phosphate.

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Marquez, Elia B., Patrick L. Gurian, Alberto Barud-Zubillaga, and Philip C. Goodell. "Correlates of Arsenic Mobilization into the Groundwater in El Paso, Texas." Air, Soil and Water Research 4 (January 2011): ASWR.S6356. http://dx.doi.org/10.4137/aswr.s6356.

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This paper addresses the contamination of groundwater by arsenic, a naturally occurring phenomenon that has caused serious cases of arsenic poisoning around the world. While a number of chemical processes are known to be capable of mobilizing arsenic, the extent to which different processes are active in actual geological settings is much less clear. In this work, the El Paso, Texas region is analyzed as a case study to better understand the factors associated with high arsenic levels in groundwater. This study includes two basins that supply drinking water to approximately 2.5 million people. The average arsenic was 8.5 ppb, which is below the current American and WHO Maximum Contaminant Level of 10 ppb. However, arsenic concentrations reached approximately 80 ppb in three different locations. Governmental archival information was combined with field water sampling, and with leaching and analysis of solid phase materials from well cuttings (sediments of the aquifers). The study identifies evidence for both competitive desorption and reductive dissolution operating to mobilize arsenic, with the importance of different mechanisms likely varying throughout the aquifers. A mean of 21% of the solid arsenic content was leached out to solution at pH 9, and mean solid phase arsenic concentration was 4.3 ppm, solid phase iron 7000 ppm, and solid carbon 0.6%, consistent with arsenic desorption out of sediments into the aqueous phase. A potential role of geothermal waters was also identified at a southern hot spot. This information is important to better understand the basic science of the arsenic geochemical cycle and may also provide a rough guide as to where low arsenic waters may be found: groundwater with high potentiometric head and short flow paths, groundwater under the influence of surface water, and lower pH groundwater.

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Sari, S. A., Z. Ujang, and U. K. Ahmad. "Geospeciation of arsenic using MINTEQA2 for a post-mining lake." Water Science and Technology 54, no. 11-12 (December 1, 2006): 289–99. http://dx.doi.org/10.2166/wst.2006.894.

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The objective of this study was to investigate the cycling of arsenic in the water column of a post-mining lake. This study is part of a research project to develop health risk assessment for the surrounding population. Inductively Coupled Plasma-Mass Spectrophotometer (ICP-MS) and Capillary Electrophoresis (CE) have been used to analyze the total amount and speciation, respectively. A computer program, called MINTEQA2, which was developed by the United States Environmental Protection Agency (USEPA) was used for predicting arsenic, iron, and manganese as functions of pH and solubility. Studying the pH values and cycle of arsenic shows that the percentage of bound arsenate, As(V) species in the form of HAsO−4 increases with range pH from 5 to 7, as well as Fe(II) and Mn(II). As expected phases of arsenic oxides are FeAsO4 and Mn3(AsO4), as a function of solubility, however none of these phases are over saturated and not precipitated. It means that the phases of arsenic oxides have a high solubility.

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Marzi, Davide, Maria Luisa Antenozio, Sara Vernazzaro, Clara Sette, Enrico Veschetti, Luca Lucentini, Giancarlo Daniele, Patrizia Brunetti, and Maura Cardarelli. "Advanced Drinking Groundwater As Phytofiltration by the Hyperaccumulating Fern Pteris vittata." Water 13, no. 16 (August 11, 2021): 2187. http://dx.doi.org/10.3390/w13162187.

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The reuse of Pteris vittata plants for multiple phytofiltration cycles is a main issue to allow an efficient phytoremediation of arsenic (As)-contaminated groundwater. Here, we assessed the capacity of phytofiltration of P. vittata plants grown for two cycles on naturally As-contaminated drinking water (collected in Central Italy), spaced by a growth cycle on non-contaminated water (N cycle). P. vittata young plants, with extensive frond and root development, were suspended individually in 15 L of water with initial As of 59 µg/L, without any additional treatment or water refilling. During cycle 1, in 45 days P. vittata plants reduced As concentration below 10 µg/L, the allowed EU limits for drinking water. During the subsequent 30 day-N cycle on non-contaminated water, no leaching of As from the roots was observed, while the water pH increased 0.9 Units, but is within the allowed limits. During cycle 2, under the same conditions as cycle 1, As concentration decreased below 10 µg/L in less than seven days. These results show that P. vittata young plants, previously used for the phytofiltration of As, do not extrude As and, when reused, remove As much more rapidly. No additional treatments were required during phytofiltration and thus this represents a sustainable, efficient, and scalable strategy.

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Navratilova, Jana, Georg Raber, Steven J. Fisher, and Kevin A. Francesconi. "Arsenic cycling in marine systems: degradation of arsenosugars to arsenate in decomposing algae, and preliminary evidence for the formation of recalcitrant arsenic." Environmental Chemistry 8, no. 1 (2011): 44. http://dx.doi.org/10.1071/en10107.

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Environmental context Despite high levels of complex organoarsenic compounds in marine organisms, arsenic in seawater is present almost entirely as inorganic species. We examine the arsenic products from a marine alga allowed to decompose under simulated natural coastal conditions, and demonstrate a multi-step conversion of organic arsenicals to inorganic arsenic. The results support the hypothesis that the arsenic marine cycle begins and ends with inorganic arsenic. Abstract Time series laboratory experiments were performed to follow the degradation of arsenic compounds naturally present in marine algae. Samples of the brown alga Ecklonia radiata, which contains three major arsenosugars, were packed into 12 tubes open to air at one end only, and allowed to naturally decompose under moist conditions. During the subsequent 25 days, single tubes were removed at intervals of 1–4 days; their contents were cut into four sections (from open to closed end) and analysed for arsenic species by HPLC/ICPMS following an aqueous methanol extraction. In the sections without direct contact with air, the original arsenosugars were degraded primarily to arsenate via two major intermediates, dimethylarsinoylethanol (DMAE) and dimethylarsinate (DMA). The section with direct contact with air degraded more slowly and significant amounts of arsenosugars remained after 25 days. We also report preliminary data suggesting that the amount of non-extractable or recalcitrant arsenic (i.e. insoluble after sequential extractions with water/methanol, acetone, and hexane) increased with time. Furthermore, we show that treatment of the pellet with 0.1-M trifluoroacetic acid at 95°C solubilises a significant amount of this recalcitrant arsenic, and that the arsenic is present mainly as a cationic species of currently unknown structure.

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Manshouri, Taghi, Subbarao V. Kala, Faramarz Ashoori, Ralph Zingaro, Emil J. Freireich, Michael Andreeff, Hagop M. Kantarjian, and Srdan Verstovsek. "Comparison of Uptake and Intracellular Induced Structural Changes of Arsenic Trioxide, an Inorganic Compound, and Organic Arsenic Derivative S-Dimethylarsino-Glutathione (SGLU; ZIO-101) in NB4 Acute Promyelocytic Leukemia (APL) Cells." Blood 106, no. 11 (November 16, 2005): 4446. http://dx.doi.org/10.1182/blood.v106.11.4446.4446.

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Abstract Arsenic trioxide (As2O3; ATO) inhibits proliferation and induces apoptosis of APL cells. However, little is known about the intracellular structural changes associated with arsenic exposure. We studied effects of 2 arsenic compounds, ATO and S-dimethylarsino-glutathione (SGLU; ZIO-101) on NB4 APL cells. ZIO-101 is novel water-soluble organic arsenic derivative currently in Phase I clinical studies. Exposure of cancer cells to ZIO-101 results in G2/M cell cycle arrest and apoptosis. NB4 cells were exposed to 10, 50, 100 and 250 μM ZIO-101 or ATO for 1 h and intracellular arsenic content was determined by inductively coupled plasma mass spectrometry (ICP/MS). ZIO-101-treated cells contained 5–8 fold more arsenic then ATO-treated cells. Electron microscopy of NB4 cells exposed to 1 μM ZIO-101 or ATO for 24–72 h revealed different structural changes. ATO treated cells showed time-dependent mitochondrial hypotrophy and apoptosis, including cytoplasmic vacuolization, nuclear condensation and cell blebs. In contrast, ZIO-101 treated cells showed time-dependent mitochondrial atrophy, mitochondrial matrix condensation, and apoptosis. These data suggest that ZIO-101 is more specific mitochondrial toxin than ATO. Studies are in progress to understand the exact mechanism through which ZIO-101 affects mitochondria. Because these arsenic derivatives have different mechanism of action they may have different spectrums of activity against cancers; this should be tested in clinical trials.

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Chen, Song-Can, Guo-Xin Sun, Yu Yan, Konstantinos T. Konstantinidis, Si-Yu Zhang, Ye Deng, Xiao-Min Li, et al. "The Great Oxidation Event expanded the genetic repertoire of arsenic metabolism and cycling." Proceedings of the National Academy of Sciences 117, no. 19 (April 29, 2020): 10414–21. http://dx.doi.org/10.1073/pnas.2001063117.

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The rise of oxygen on the early Earth about 2.4 billion years ago reorganized the redox cycle of harmful metal(loids), including that of arsenic, which doubtlessly imposed substantial barriers to the physiology and diversification of life. Evaluating the adaptive biological responses to these environmental challenges is inherently difficult because of the paucity of fossil records. Here we applied molecular clock analyses to 13 gene families participating in principal pathways of arsenic resistance and cycling, to explore the nature of early arsenic biogeocycles and decipher feedbacks associated with planetary oxygenation. Our results reveal the advent of nascent arsenic resistance systems under the anoxic environment predating the Great Oxidation Event (GOE), with the primary function of detoxifying reduced arsenic compounds that were abundant in Archean environments. To cope with the increased toxicity of oxidized arsenic species that occurred as oxygen built up in Earth’s atmosphere, we found that parts of preexisting detoxification systems for trivalent arsenicals were merged with newly emerged pathways that originated via convergent evolution. Further expansion of arsenic resistance systems was made feasible by incorporation of oxygen-dependent enzymatic pathways into the detoxification network. These genetic innovations, together with adaptive responses to other redox-sensitive metals, provided organisms with novel mechanisms for adaption to changes in global biogeocycles that emerged as a consequence of the GOE.

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Schiller, Gary J., James Slack, John D. Hainsworth, James Mason, Mansoor Saleh, David Rizzieri, Dan Douer, and Alan F. List. "Phase II Multicenter Study of Arsenic Trioxide in Patients With Myelodysplastic Syndromes." Journal of Clinical Oncology 24, no. 16 (June 1, 2006): 2456–64. http://dx.doi.org/10.1200/jco.2005.03.7903.

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Purpose To evaluate the efficacy and safety of arsenic trioxide monotherapy in patients with myelodysplastic syndromes (MDS). Patients and Methods Patients received arsenic trioxide (0.25 mg/kg/d) on 5 consecutive days per week for 2 weeks, followed by 2 weeks’ rest (one cycle). Two patient cohorts were established according to International Prognostic Scoring System risk category: lower-risk (low or intermediate-1) or higher-risk MDS (intermediate-2 or high). For lower-risk MDS, hematologic improvement (HI) was the primary response end point. For higher-risk MDS, additional end points included complete or partial remission. Based on the expected time to response, patients receiving two or more cycles were prospectively evaluated. Results Hematologic adverse events included neutropenia, thrombocytopenia, and febrile neutropenia. Two patients died during the study due to treatment-related toxicities. Most common grade 3/4 nonhematologic events were pneumonia, fatigue, hemorrhage, pain, and dyspnea. Among patients who received one or more doses (n = 70) or completed two or more cycles (n = 51), the HI rates were 34% and 39% in lower-risk patients, and 6% and 9% in higher-risk patients, respectively; the overall major HI rates were 20% and 22%. One higher-risk patient achieved a complete remission (3%). Major HIs were observed in all hematologic lineages; erythroid responses were the most common. Transfusion independence or reduction by ≥ 50% occurred in 33% of patients dependent on RBC transfusions. The overall median duration of HI was 6.8 months (range, 2 to 40 months). Conclusion Arsenic trioxide monotherapy has moderate activity against MDS, with a manageable adverse effect profile. The further study of arsenic trioxide in MDS, particularly in combination with other agents, is warranted.

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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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Vega, Silvia, Jan Weijma, and Cees N. J. Buisman. "Immobilization of Arsenic by a Thermoacidophilic Mixed Culture with Pyrite as Energy Source." Solid State Phenomena 262 (August 2017): 656–59. http://dx.doi.org/10.4028/www.scientific.net/ssp.262.656.

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Arsenic is an abundant element associated with a wide range of minerals and a major contaminant in metallurgical wastewater. For the immobilization of arsenic, iron arsenate in the very stable mineral scorodite (FeAsO4 2H2O) is the preferred route. Microorganisms of the natural iron cycle living at pH below 2 and high temperatures can conduct the oxidation of ferrous iron with oxygen, which is not feasible chemically at these extreme conditions. Remarkably, at similar acidic conditions and high temperature these microorganisms can also carry out the oxidation of arsenite (As(III)) to arsenate (As(V)). Using these intrinsic features of the microorganisms, we have investigated the role of a thermoacidophilic mixed culture in the oxidation of As(III) and precipitation of (As(V) in the form of scorodite from a synthetic wastewater containing 6.7mM of As(III) and 0.5%Wt pyrite as main iron Fe(II) source. The results indicate that As(III) was completely oxidized from the synthetic wastewater in the presence of pyrite and scorodite was formed only in presence of the mixed culture at a Fe/As:1.3. This is a combination of biological oxidation and biocrystallisation accomplished to the presence of pyrite not only as the main energy source for the microorganisms, but as catalyst in the As(III) oxidation reaction.

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Berenson, James, Jeff Matous, Delina Ferretti, Regina Swift, Russell Mapes, Blake Morrison, Howard Yeh, and Sal Bevivino. "A Phase I/II Trial Evaluating the Combination of Arsenic Trioxide, Bortezomib and Ascorbic Acid for Patients with Relapsed or Refractory Multiple Myeloma." Blood 106, no. 11 (November 16, 2005): 2565. http://dx.doi.org/10.1182/blood.v106.11.2565.2565.

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Abstract Background: Both arsenic trioxide and bortezomib as single agents have shown efficacy for patients with relapsed/refractory multiple myeloma (MM). Recently, we have demonstrated synergistic anti-MM effects when these two agents are combined to treat human MM in SCID mice and evaluated in in vitro studies. In addition, we and others have also shown that the addition of ascorbic acid (AA) sensitizes MM cells to the cytotoxic effects of arsenic trioxide both through in vitro and in vivo studies. Thus, the objective of the current Phase I clinical trial was to assess the safety and tolerability of bortezomib + arsenic trioxide + AA treatment for patients with refractory/relapsed MM. Methods: A treatment cycle comprised of intravenous injections of arsenic trioxide, bortezomib and AA on days 1, 4, 8, and 11 followed by a 10-day rest period every three weeks. Bortezomib was given at one of three dose levels (0.7, 1.0, or 1.3 mg/m2), followed by arsenic trioxide at one of two doses (0.125 or 0.25 mg/kg) intravenously followed by AA (1000 mg). Patients were treated for a maximum of eight cycles and were eligible for maintenance therapy with the same treatments given once every other week. Results: Eighteen patients have been enrolled to date, with three patients enrolled in each of the six cohorts. Patients had received a median of three prior therapies (range, 1–6), and five patients had received prior bortezomib therapy. Fifteen patients are evaluable for efficacy to date, and response data are summarized in Table 1. Overall, among the 15 evaluable patients, seven patients responded (2 PR, 5 MR), three patients showed stable disease, and five patients progressed. Among the six patients (in cohorts 1 and 4) enrolled at the lowest (0.7 mg/m2) bortezomib dose level, only one achieved a MR whereas among the nine evaluable patients enrolled at the higher (1.0 and 1.3 mg/m2) bortezomib dose levels six patients responded (2 PR, 4 MR). In general, the regimen was well tolerated. One patient in cohort 3 was removed from study during the first cycle because of the development of an asymptomatic arrhythmia which resolved spontaneously. Other serious adverse events included pneumonia in two patients, chest pain, and abdominal pain (one patient each). Conclusion: These early results from this Phase I/II study indicate that the combination of bortezomib, arsenic trioxide and ascorbic acid has efficacy and is well tolerated in a heavily pretreated population of patients with relapsed or refractory MM. Because of these encouraging clinical results, we plan to further evaluate this combination in a larger group of patients with relapsed/refractory myeloma. Table 1. Dose escalation scheme Cohorts Arsenic trioxide Bortezomib No. of evaluable pts Response *one patient in cohort 3 went off study during cycle 1 (see above), and the other two patients (one each in cohorts 3 and 6) are too early for response evaluation Cohort 1 0.125 mg/kg 0.7 mg/m2 3 1 MR, 2 PD Cohort 2 0.125 mg/kg 1.0 mg/m2 3 1 PR, 1 SD, 1 PD Cohort 3 0.125 mg/kg 1.3 mg/m2 1* 1 PR Cohort 4 0.25 mg/kg 0.7 mg/m2 3 1 SD, 2 PD Cohort 5 0.25 mg/kg 1.0 mg/m2 3 3 MR Cohort 6 0.25 mg/kg 1.3 mg/m2 2* 1 SD, 1 MR

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Yen, James L., Ning-Yuan Su, and Peter Kaiser. "The Yeast Ubiquitin Ligase SCFMet30Regulates Heavy Metal Response." Molecular Biology of the Cell 16, no. 4 (April 2005): 1872–82. http://dx.doi.org/10.1091/mbc.e04-12-1130.

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Cells have developed a variety of mechanisms to respond to heavy metal exposure. Here, we show that the yeast ubiquitin ligase SCFMet30plays a central role in the response to two of the most toxic environmental heavy metal contaminants, namely, cadmium and arsenic. SCFMet30inactivates the transcription factor Met4 by proteolysis-independent polyubiquitination. Exposure of yeast cells to heavy metals led to activation of Met4 as indicated by a complete loss of ubiquitinated Met4 species. The association of Met30 with Skp1 but not with its substrate Met4 was inhibited in cells treated with cadmium. Cadmium-activated Met4 induced glutathione biosynthesis as well as genes involved in sulfuramino acid synthesis. Met4 activation was important for the cellular response to cadmium because mutations in various components of the Met4-transcription complex were hypersensitive to cadmium. In addition, cell cycle analyses revealed that cadmium induced a delay in the transition from G1to S phase of the cell cycle and slow progression through S phase. Both cadmium and arsenic induced phosphorylation of the cell cycle checkpoint protein Rad53. Genetic analyses demonstrated a complex effect of cadmium on cell cycle regulation that might be important to safeguard cellular and genetic integrity when cells are exposed to heavy metals.

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Chung, Chi-Jung, Chi-Jung Huang, Yeong-Shiau Pu, Chien-Tien Su, Yung-Kai Huang, Ying-Ting Chen, and Yu-Mei Hsueh. "Polymorphisms in cell cycle regulatory genes, urinary arsenic profile and urothelial carcinoma." Toxicology and Applied Pharmacology 232, no. 2 (October 2008): 203–9. http://dx.doi.org/10.1016/j.taap.2008.06.011.

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Rodriguez, Mildred, Susana Pinto-Castilla, Myloa Morgado-Vargas, and Paulino Betancourt. "Influence of arsenic on light cycle oil hydrodesulfurization over a CoMo catalyst." Reaction Kinetics, Mechanisms and Catalysis 131, no. 1 (September 2, 2020): 199–211. http://dx.doi.org/10.1007/s11144-020-01856-y.

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Manna, Biswa Ranjan, Soumen Dey, Sushanta Debnath, and Uday Chand Ghosh. "Removal of Arsenic from Groundwater using Crystalline Hydrous Ferric Oxide (CHFO)." Water Quality Research Journal 38, no. 1 (February 1, 2003): 193–210. http://dx.doi.org/10.2166/wqrj.2003.013.

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Abstract Synthesis of crystalline hydrous ferric oxide (CHFO), a modified iron-based adsorbent, and its arsenic sorption behaviour have been reported. Here, the effects of pH with variation of arsenic concentrations, contact time, pre-drying of CHFO, competition of some other anions and regeneration of arsenicsaturated CHFO are conducted by batch method. The sorption of As(V) is highly dependent on the concentration and pH of the experimental system, while that for As(III) is pH insensitive. As(III) is found to require less contact time to attain equilibrium than that of arsenic(V). Pre-drying of CHFO in the temperature range of 200 to 300°C is found to be effective in removing both As(III) and As(V). Adsorption kinetics follow the first-order Lagergren model. The equilibrium data conform to the Langmuir isotherm. Evaluated Langmuir constants and equilibrium parameter (RL) indicate that CHFO is a better As(III) adsorbent under experimental conditions. Sulphate, phosphate and bicarbonate compete poorly with As(III) sorption. A field test using CHFO-packed fixed-bed column is reported. Effluent water bed volumes of 14,000, 11,000 and 9000 BV (arsenic ≤ 0.01 mg L-1) were obtained in the first, second and third cycle of operation from a groundwater sample (arsenic content: 320.400 μg L-1). Regeneration of the exhausted column was achieved with up to 80 to 85% efficiency using 3 BV of 5 M NaOH solution recycled through the column five times. Arsenic was recovered as As2S3 from the regenerates, to avoid recycling of arsenic into the environment.

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Ye, Yongbin, Xiaojun Xu, and Qifa Liu. "Leukemia Stem-like KG-1a Cells Escape the Synergistic Cytotoxic Effect of Arsenic Trioxide and Aclacinomycin: Regulated By Survivin." Blood 128, no. 22 (December 2, 2016): 5248. http://dx.doi.org/10.1182/blood.v128.22.5248.5248.

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Abstract Leukemia stem-like KG-1a cells escape the synergistic cytotoxic effect of arsenic trioxide and aclacinomycin: regulated by survivin Yongbin YE1 , Xiaojun.XU1 , Liu Qifa2 Correspondence to: Xiaojun XU. E-mail: doctorxu@163.com 1Department of Hematology, Zhongshan Hospital of Sun Yat-sen University & Zhongshan City People Hospital, Zongshan 528403 2Department of Hematology, Nanfang Hospital of Southern Medical University, Guangzhou,510515 Abstract AIM OF STUDY: Arsenic trioxide combined with aclacinomycin has a synergistic cytotoxic effect on leukemia stem cell-like cells KG-1a in our pervious study, however, there are still a part of KG-1a cells escaped the synergistic cytotoxicity, survivin may plays in a key role in this process. In this study, we have studied the interaction and mechanism of survivin in regulating leukemia stem-like KG-1a cell escape the synergistic cytotoxic effect of arsenic trioxide and aclacinomycin. MATERIALS AND METHODS: The anti-proliferation effect was detected by CCK-8 and colony-forming assay, protein-protein chip assay was used to analysis the expression level of survivin before and after combination treatment. The induction of apoptosis and cell cycle arrest in KG-1a cell line were detected by FACS, the expression of related signal pathway protein was detected by western blot. RESULTS: The anti-proliferation of KG-1a cells caused by arsenic trioxide or aclacinomycin showed a time- and dose-independent manner. However, protein-protein chip assay showed that the expression of survivin had a significant increase after the combination treatment (p<0.05), but when survivin was suppressed, the apoptosis rate had a more significant increase than the single drug treatment. Meanwhile, more prominent cell cycle arrest was observed in the combination treatment, further study found that suppression of survivin combined with chemotherapy may activate the related apoptosis pathway protein but suppress the PI3K/AKT signal pathway. CONCLUSION: survivin play an important role in regulating leukemia stem cell escape the synergistic cytotoxic effect of arsenic trioxide and aclacinomycin. The mechanism of regulation process may through activate the related apoptosis pathway protein and supperss the PI3K/AKT signal pathway. This study may provide a further benefit for reversing chemotherapy resistant for acute leukemia Key words: arsenic trioxide,aclacinomycin, Acute leukemia; survivin; chemotherapy resistant Disclosures No relevant conflicts of interest to declare.

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Journal articles on the topic 'Arsenic cycle'

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