Experimental and Theoretical Characterization of Arsenite in Water:  Insights into the Coordination Environment of As−O

Ramı́rez-Solı́s, A.; Mukopadhyay, Rita; Rosen, Barry P.; Stemmler, Timothy L.

doi:10.1021/ic0351592

Cited by 129 publications

(95 citation statements)

References 12 publications

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“…However, studies have shown that arsenic in the form of arsenic trihydroxide (As(OH) 3 ), the water soluble form of arsenite, enters cells rapidly through human aquaglyceroporins (hAQP9 and hAQP7) (Liu et al, 2004). In addition, non-ionic arsenite transport appears to be involved in the cellular uptake process while ionic transport does not (Ramirez-Solis et al, 2004). We have shown that arsenite accumulates in A375 and SK-Mel-28 cells and that inhibition of arsenite detoxification and metabolism increases arsenic accumulation (McNeely et al, 2008).…”

Section: Resultsmentioning

confidence: 99%

“…Every mole of ATO in solution is equivalent to 2 moles of sodium arsenite. The most stable structure of trivalent arsenic oxides existing in solution at neutral pH is As(OH) 3 (Ramirez-Solis et al, 2004). Therefore we used sodium arsenite in all experiments for its convenience, ease of use, and identical structure of ATO and sodium arsenite in solution.…”

Section: Cell Culture and Specialty Chemicalsmentioning

confidence: 99%

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Arsenite-induced mitotic death involves stress response and is independent of tubulin polymerization

Taylor

McNeely

Miller

et al. 2008

Toxicology and Applied Pharmacology

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Arsenite, a known mitotic disruptor, causes cell cycle arrest and cell death at anaphase. The mechanism causing mitotic arrest is highly disputed. We compared arsenite to the spindle poisons nocodazole and paclitaxel. Immunofluorescence analysis of α-tubulin in interphase cells demonstrated that, while nocodazole and paclitaxel disrupt microtubule polymerization through destabilization and hyperpolymerization, respectively, microtubules in arsenite-treated cells remain comparable to untreated cells even at supra-therapeutic concentrations. Immunofluorescence analysis of α-tubulin in mitotic cells showed spindle formation in arsenite-and paclitaxel-treated cells but not in nocodazole-treated cells. Spindle formation in arsenite-treated cells appeared irregular and multi-polar. γ-tubulin staining showed that cells treated with nocodazole and therapeutic concentrations of paclitaxel contained two centrosomes. In contrast, most arsenite-treated mitotic cells contained more than two centrosomes, similar to centrosome abnormalities induced by heat shock. Of the three drugs tested, only arsenite treatment increased expression of the inducible isoform of heat shock protein 70 (HSP70i). HSP70 and HSP90 proteins are intimately involved in centrosome regulation and mitotic spindle formation. HSP90 inhibitor 17-DMAG sensitized cells to arsenite treatment and increased arsenite-induced centrosome abnormalities. Combined treatment of 17-DMAG and arsenite resulted in a supra-additive effect on viability, mitotic arrest, and centrosome abnormalities. Thus, arsenite-induced abnormal centrosome amplification and subsequent mitotic arrest is independent of effects on tubulin polymerization and may be due to specific stresses that are protected against by HSP90 and HSP70.

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Section: Resultsmentioning

confidence: 99%

Section: Cell Culture and Specialty Chemicalsmentioning

confidence: 99%

Arsenite-induced mitotic death involves stress response and is independent of tubulin polymerization

Taylor

McNeely

Miller

et al. 2008

Toxicology and Applied Pharmacology

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“…Arsenic trioxide, which is As 2 O 3 in the solid, anhydrous form and As (OH) 3 in solution at physiological pH [4], is used clinically as a chemotherapeutic drug for treatment of acute promyelocytic leukemia [5]. Although epidemiological studies demonstrated that arsenic exposure is associated with a high frequency of circulatory and neurological problems [2,6,7], how arsenic causes non-cancer-related diseases is far from clear.…”

Section: Introductionmentioning

confidence: 99%

Mammalian glucose permease GLUT1 facilitates transport of arsenic trioxide and methylarsonous acid

Liu

Sánchez

Jiang

et al. 2006

Biochemical and Biophysical Research Communications

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121

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Arsenic exposure is associated with hypertension, diabetes and cancer. Some mammals methylate arsenic. Saccharomyces cerevisiae hexose permeases catalyze As(OH) 3 uptake. Here we report that mammalian glucose transporter GLUT1 catalyzes As(OH) 3 and CH 3 As(OH) 2 uptake in yeast or in Xenopus laevis öocytes. Expression of GLUT1 in a yeast lacking other glucose transporters allows for growth on glucose. Yeast expressing yeast HXT1 or rat GLUT1 transport As(OH) 3 and CH 3 As (OH) 2 . The K m of GLUT1 is to 1.2 mM for CH 3 As(OH) 2 , compared to a K m of 3 mM for glucose. Inhibition between glucose and CH 3 As(OH) 2 is noncompetitive, suggesting differences between the translocation pathways of hexoses and arsenicals. Both human and rat GLUT1 catalyze uptake of both As(OH) 3 and CH 3 As(OH) 2 in öocytes. Thus GLUT1 may be a major pathway uptake of both inorganic and methylated arsenicals in erythrocytes or the epithelial cells of the blood-brain barrier, contributing to arsenic-related cardiovascular problems and neurotoxicity.Arsenic ranks first on the United States Government's Comprehensive Environmental Response, Compensation, and Liability (Superfund) Act Priority List of Hazardous Substances . In response to the Safe Water Drinking Act, the United States Environmental Protection Agency has set the allowable level of arsenic in drinking water at 10 ppb , which is less than the level in the water supplies of many U.S. municipalities . In addition, the Environmental Protection Agency's Office of Pesticide Programs is concerned with exposure to the organic arsenicals methylarsenic acid and dimethylarsenic acid, pentavalent arsenicals used as pesticides and herbicides .Health effects associated with arsenic exposure include cardiovascular and peripheral vascular disease, neurological disorders, diabetes mellitus and various cancers, including liver, bladder, kidney and skin [1][2][3]. Arsenic trioxide, which is As 2 O 3 in the solid, anhydrous form and As (OH) 3 in solution at physiological pH [4], is used clinically as a chemotherapeutic drug for treatment of acute promyelocytic leukemia [5]. Although epidemiological studies demonstrated that arsenic exposure is associated with a high frequency of circulatory and neurological problems [2,6,7], how arsenic causes non-cancer-related diseases is far from clear. Here we report that GLUT1 facilitates uptake of As(OH) 3 and CH 3 As(OH) 2 using heterologous expression in S. cerevisiae and X. laevis öocytes. S. cerevisiae is a valuable model system for structure-function studies of mammalian membrane proteins such as GLUT1 [22,23]. A yeast strain with low uptake of As(OH) 3 and CH 3 As(OH) 2 was constructed by deletion of all 18 hexose transporters, FPS1, which encodes an aquaglyceroporin that facilitates As(OH) 3 influx, and ACR3, the gene for an...

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“…Most plants appear to have high levels of endogenous arsenate reductase activity, which reduces Ͼ95% of the arsenate they take up to arsenite (5,8). Arsenite, which at neutral pH contains arsenic in the trivalent oxidation state [As(III)], and probably as the acid HAsO 3 2Ϫ , is highly reactive and readily forms As(III)-thiol complexes (9). It appears that in most plants, arsenite is sequestered in roots, preventing it from moving up into stems, leaves, and reproductive organs.…”

mentioning

confidence: 99%

Hyperaccumulation of arsenic in the shoots of Arabidopsis silenced for arsenate reductase (ACR2)

Dhankher

Rosen

McKinney

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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237

144

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Endogenous plant arsenate reductase (ACR) activity converts arsenate to arsenite in roots, immobilizing arsenic below ground. By blocking this activity, we hoped to construct plants that would mobilize more arsenate aboveground. We have identified a single gene in the Arabidopsis thaliana genome, ACR2, with moderate sequence homology to yeast arsenate reductase. Expression of ACR2 cDNA in Escherichia coli complemented the arsenate-resistant and arsenate-sensitive phenotypes of various bacterial ars operon mutants. RNA interference reduced ACR2 protein expression in Arabidopsis to as low as 2% of wild-type levels. The various knockdown plant lines were more sensitive to high concentrations of arsenate, but not arsenite, than wild type. The knockdown lines accumulated 10-to 16-fold more arsenic in shoots (350 -500 ppm) and retained less arsenic in roots than wild type, when grown on arsenate medium with <8 ppm arsenic. Reducing expression of ACR2 homologs in tree, shrub, and grass species should play a vital role in the phytoremediation of environmental arsenic contamination.Escherichia coli ArsC ͉ drinking water ͉ CDC25 ͉ toxicant ͉ arsenic pollution E nvironmental arsenic pollution is widely recognized as a global health problem (1) (www.epa.gov͞ogwdw͞ars͞arsenic.html). High levels of arsenic in soil and drinking water have been reported around the world, but the situation is worst in India and Bangladesh, where Ͼ400 million people are at risk of arsenic poisoning (2). The World Health Organization predicts that long-term exposure to arsenic could reach epidemic proportions, estimating that 1 in 10 people in the most contaminated areas may ultimately die from diseases related to arsenic poisoning (3). The high financial cost associated with repairing the environmental damage by using physical remediation methods such as excavation and reburial make these technologies unacceptable for cleaning up the vast areas of the planet that need arsenic remediation. As a result, the overwhelming majority of arsenic-contaminated sites are not being cleaned up.Phytoremediation is the use of plants to clean up environmental pollutants and is considered an important alternative to physical methods for cleaning up arsenic (4). Our objective is to develop a genetics-based arsenic phytoremediation strategy that can be used in any plant species. Plants that hyperaccumulate arsenic to high levels aboveground would be harvested and the arsenic further concentrated by incineration. In previous studies, we engineered model plants expressing a bacterial arsenate reductase (ArsC; EC 1.20.4.1) aboveground and constitutively expressing ␥-glutamylcysteine synthetase (5). By reducing arsenate to arsenite in leaves and trapping arsenite in thiol-peptide complexes, these plants accumulate 3-fold more arsenic aboveground than wild type and are also highly tolerant to toxic levels of arsenic. The research described herein extends these observations and attacks a particular problem limiting the engineered phytoremediation of arsenic: its transpor...

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Experimental and Theoretical Characterization of Arsenite in Water: Insights into the Coordination Environment of As−O

Cited by 129 publications

References 12 publications

Arsenite-induced mitotic death involves stress response and is independent of tubulin polymerization

Arsenite-induced mitotic death involves stress response and is independent of tubulin polymerization

Mammalian glucose permease GLUT1 facilitates transport of arsenic trioxide and methylarsonous acid

Hyperaccumulation of arsenic in the shoots of Arabidopsis silenced for arsenate reductase (ACR2)

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