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PubMed1987

Effects of arsenate on the Ca2+ ATPase of sarcoplasmic reticulum.

The effect of arsenate on the partial reactions of the catalytic cycle of the Ca2+ ATPase of skeletal muscle of sarcoplasmic reticulum was studied. With the use of native vesicles it was found that arsenate accelerates the rate of ITP hydrolysis and inhibits both Ca2+ or Sr2+ uptake. These effects were not observed when ATP was used as substrate or, with the use of ITP, when leaky vesicles were assayed. Activation of ITP hydrolysis is related to an increase of the enzyme's apparent affinity for ITP. Arsenate increases the steady-state level of the phosphoenzyme formed from ITP. This depends on the concentration of both Pi and Ca2+, in the medium. Ca2+ and Sr2+ efflux were accelerated by arsenate. The fast Ca2+ efflux promoted by arsenate is impaired by external Ca2+. Arsenate competes with Pi for the phosphorylating site of the enzyme.

Adenosine Triphosphate↗
PubMed2006

Dissimilatory arsenate and sulfate reduction in sediments of two hypersaline, arsenic-rich soda lakes: Mono and Searles Lakes, California.

A radioisotope method was devised to study bacterial respiratory reduction of arsenate in sediments. The following two arsenic-rich soda lakes in California were chosen for comparison on the basis of their different salinities: Mono Lake (approximately 90 g/liter) and Searles Lake (approximately 340 g/liter). Profiles of arsenate reduction and sulfate reduction were constructed for both lakes. Reduction of [73As]arsenate occurred at all depth intervals in the cores from Mono Lake (rate constant [k] = 0.103 to 0.04 h(-1)) and Searles Lake (k = 0.012 to 0.002 h(-1)), and the highest activities occurred in the top sections of each core. In contrast, [35S]sulfate reduction was measurable in Mono Lake (k = 7.6 x10(4) to 3.2 x 10(-6) h(-1)) but not in Searles Lake. Sediment DNA was extracted, PCR amplified, and separated by denaturing gradient gel electrophoresis (DGGE) to obtain phylogenetic markers (i.e., 16S rRNA genes) and a partial functional gene for dissimilatory arsenate reduction (arrA). The amplified arrA gene product showed a similar trend in both lakes; the signal was strongest in surface sediments and decreased to undetectable levels deeper in the sediments. More arrA gene signal was observed in Mono Lake and was detectable at a greater depth, despite the higher arsenate reduction activity observed in Searles Lake. A partial sequence (about 900 bp) was obtained for a clone (SLAS-3) that matched the dominant DGGE band found in deeper parts of the Searles Lake sample (below 3 cm), and this clone was found to be closely related to SLAS-1, a novel extremophilic arsenate respirer previously cultivated from Searles Lake.

Arsenates↗
PubMed2006

Sulfide oxidation coupled to arsenate reduction by a diverse microbial community in a soda lake.

We characterized the arsenate-reducing, sulfide-oxidizing population of Mono Lake, California, by analyzing the distribution and diversity of rrnA, cbbL, and dissimilatory arsenate reductase (arrA) genes in environmental DNA, arsenate-plus sulfide-amended lake water, mixed cultures, and isolates. The arsenate-reducing community was diverse. An organism represented by an rrnA sequence previously retrieved from Mono Lake and affiliated with the Desulfobulbaceae (Deltaproteobacteria) appears to be an important member of the arsenate-reducing, sulfide-oxidizing community. Sulfide oxidation coupled with arsenate reduction appears to proceed via a two-electron transfer, resulting in the production of arsenite and an intermediate S compound that is subsequently disproportionated. A realgar-like As/S mineral was formed in some experiments.

Arsenates↗
PubMed1998

The ars operon in the skin element of Bacillus subtilis confers resistance to arsenate and arsenite.

The Bacillus subtilis skin element confers resistance to arsenate and arsenite. The ars operon in the skin element contains four genes in the order arsR, ORF2, arsB, and arsC. Three of these genes are homologous to the arsR, arsB, and arsC genes from the staphylococcal plasmid pI258, while no homologs of ORF2 have been found. Inactivation of arsR, arsB, or arsC results in either constitutive expression of ars, an arsenite- and arsenate-sensitive phenotype, or an arsenate-sensitive phenotype, respectively. These results suggest that ArsR, ArsB, and ArsC function as a negative regulator, a membrane-associated protein need for extrusion of arsenite, and arsenate reductase, respectively. Expression of the ars operon was induced by arsenate, arsenite, and antimonite. Northern hybridization and primer extension analysis showed that synthesis of a full-length ars transcript of about 2.4 kb was induced by arsenate and that the ars promoter contains sequences that resemble the -10 and -35 regions of promoters that are recognized by E sigmaA.

Adenosine Triphosphatases↗
PubMed2003

Inherited resistance to arsenate toxicity in two populations of Lumbricus rubellus.

No unequivocal evidence exists of genetically inherited resistance to metals/metalloids in field populations of earthworms. We studied cocoon production in adult Lumbricus rubellus Hoffmeister collected from an abandoned arsenic and copper mine (Devon Great Consols, Devon, UK), and abandoned tungsten mine (Carrock Fell, Cumbria, UK) and an uncontaminated cultured population. The earthworms were kept in uncontaminated soil for nine weeks. From a total of 42 L. rubellus from each site, Devon Great Consols adults produced 301 cocoons, of which 42 were viable; Carrock Fell 60 cocoons, of which 11 were viable; and the reference population 101 cocoons, of which 62 were viable. The hatchlings were collected and stored at 4 degrees C at weekly intervals. After 12 weeks, all hatchlings were transferred to clean soil and maintained at 15 degrees C for 20 weeks until they showed evidence of a clitellum. In toxicity trials, F1 generation L. rubellus were exposed to 2,000 mg As/kg as sodium arsenate or 300 mg Cu/kg as copper chloride for 28 d. The F1 generation L. rubellus from Devon Great Consols mine demonstrated resistance to arsenate but not copper. All L. rubellus from Devon Great Consols kept in soil treated with sodium arsenate remained in good condition over the 28-d period but lost condition rapidly and suffered high mortality in soil treated with copper chloride. The control population suffered high mortality in soil treated with sodium arsenate and copper chloride. Previous work has shown that field-collected adults demonstrate resistance to both arsenate and Cu toxicity under these conditions. Thus, while arsenate resistance may be demonstrated in F1 generation L. rubellus from one of the contaminated sites, Cu resistance is not. The F1 adults and F2 cocoons did not have significantly higher levels of As than the control population, with no residual As tissue burden, suggesting that resistance to As in these populations may be inherited.

Adaptation, Physiological↗
PubMed1983

Metabolism and renal handling of sodium arsenate in dogs.

Renal handling of sodium arsenate was studied in 5 dogs. Using a low dose (0.73 mg/kg of body weight) of sodium arsenate given IV, variable arsenite concentrations were detected in plasma and urine. Using a medium dose (7.33 mg/kg), the renal tubule cells were determined to be the probable sites of reabsorption of arsenate, reduction of arsenate to arsenite, and secretion or diffusion of the latter into urine. However, using a high dose (14.66 mg/kg), despite a similar pattern of reduction of arsenate to arsenite, marked reabsorption of arsenite into plasma took place instead of secretion or diffusion into urine. Because of reabsorption, the amount of arsenite in plasma (18.4 +/- 3.5% of the total As) was about 3 times higher than that measured during the medium dose experiment (6.0 +/- 1.0%). During the clearance experiments which lasted 110 minutes, only 40% to 45% of the arsenate infused was excreted in urine, and a minimal amount of dimethylarsinic acid (DMAA) was detected. In contrast, by the next day, DMAA was the major metabolite excreted in urine. This excretion of As as DMAA was partly due to delayed excretion of 55% to 60% As that was stored in the body and was subsequently metabolized.

Animals↗
PubMed2005

Effects of pH and ionic strength on the adsorption of phosphate and arsenate at the goethite-water interface.

The surface properties of a well-crystallized synthetic goethite have been studied by acid-base potentiometric titrations, electrophoresis, and phosphate and arsenate adsorption isotherms at different pH and electrolyte concentrations. The PZC and IEP of the studied goethite were 9.3+/-0.1 and 9.3+/-0.2, respectively. Phosphate and arsenate adsorption decrease as the pH increases in either 0.1 or 0.01 M KNO(3) solutions. Phosphate adsorption is more sensitive to changes in pH and ionic strength than that of arsenate. The combined effects of pH and ionic strength result in higher phosphate adsorption in acidic media at most ionic strengths, but result in lower phosphate adsorption in basic media and low ionic strengths. The CD-MUSIC model yields rather good fit of the experimental data. For phosphate it was necessary to postulate the presence of three inner-sphere surface complexes (monodentate nonprotonated, bidentate nonprotonated, and bidentate protonated). In contrast, arsenate could be well described by postulating only the presence of the two bidenate species. A small improvement of the arsenate adsorption data could be achieved by assuming the presence of a monodentate protonated species. Model predictions are in agreement with spectroscopic evidence, which suggest, especially for the case of arsenate, that mainly bidentate inner-sphere complexes are formed at the goethite-water interface.

Journal Article↗
PubMed2006

Interplay between ion binding and catalysis in the thioredoxin-coupled arsenate reductase family.

In the thioredoxin (Trx)-coupled arsenate reductase family, arsenate reductase from Staphylococcus aureus plasmid pI258 (Sa_ArsC) and from Bacillus subtilis (Bs_ArsC) are structurally related detoxification enzymes. Catalysis of the reduction of arsenate to arsenite involves a P-loop (Cys10Thr11Gly12Asn13Ser14Cys15Arg16) structural motif and a disulphide cascade between three conserved cysteine residues (Cys10, Cys82 and Cys89). For its activity, Sa_ArsC benefits from the binding of tetrahedral oxyanions in the P-loop active site and from the binding of potassium in a specific cation-binding site. In contrast, the steady-state kinetic parameters of Bs_ArsC are not affected by sulphate or potassium. The commonly occurring mutation of a histidine (H62), located about 6 A from the potassium-binding site in Sa_ArsC, to a glutamine uncouples the kinetic dependency on potassium. In addition, the binding affinity for potassium is affected by the presence of a lysine (K33) or an aspartic acid (D33) in combination with two negative charges (D30 and E31) on the surface of Trx-coupled arsenate reductases. In the P-loop of the Trx-coupled arsenate reductase family, the peptide bond between Gly12 and Asn13 can adopt two distinct conformations. The unique geometry of the P-loop with Asn13 in beta conformation, which is not observed in structurally related LMW PTPases, is stabilized by tetrahedral oxyanions and decreases the pK(a) value of Cys10 and Cys82. Tetrahedral oxyanions stabilize the P-loop in its catalytically most active form, which might explain the observed increase in k(cat) value for Sa_ArsC. Therefore, a subtle interplay of potassium and sulphate dictates the kinetics of Trx-coupled arsenate reductases.

Amino Acid Sequence↗
PubMed1994

Properties of the arsenate reductase of plasmid R773.

Resistance to toxic oxyanions in Escherichia coli is conferred by the ars operon carried on plasmid R773. The gene products of this operon catalyze extrusion of antimonials and arsenicals from cells of E. coli, thus providing resistance to those toxic oxyanions. In addition, resistance to arsenate is conferred by the product of the arsC gene. In this report, purified ArsC protein was shown to catalyze reduction of arsenate to arsenite. The enzymatic activity of the ArsC protein required glutaredoxin as a source of reducing equivalents. Other reductants, including glutathione and thioredoxin, were not effective electron donors. A spectrophotometric assay was devised in which arsenate reduction was coupled to NADPH oxidation. The results obtained with the coupled assay corresponded to those found by direct reduction of radioactive arsenate to arsenite. The only substrate of the reaction was arsenate (Km = 8 mM); other oxyanions including phosphate, sulfate, and antimonate were not reduced. Phosphate and sulfate were weak inhibitors, while the product, arsenite, was a stronger inhibitor (Ki = 0.1 mM). Arsenate reductase activity exhibited a pH optimum of 6.3-6.8. These results indicate that the ArsC protein is a novel reductase, and elucidation of its enzymatic mechanism should be of interest.

Adenosine Triphosphatases↗
PubMed1973

Continuous culture of Rhodotorula rubra: kinetics of phosphate-arsenate uptake, inhibition, and phosphate-limited growth.

The pink yeast Rhodotorula rubra of marine origin was found to be capable of extended growth at very low phosphate concentrations (K(0.5) = 10.8 nm). Average intracellular phosphate concentrations, based on isotope exchange techniques, were 15 to 200 nm, giving concentration gradients across the cell envelope of about 10(6). Sensitivity to metabolic inhibitors occurred at micromolar concentrations. Inability of the phosphate transport system, K(s) = 0.5 to 2.8 mum, V(max) = 55 mumoles per g of cells per min, to discriminate against arsenate transport led to arsenate toxicity at 1 to 10 nm, whereas environmental arsenate levels are reportedly much higher. Phosphate competitively prevented arsenate toxicity. The K(i) for phosphate inhibition of arsenate uptake was 0.7 to 1.2 mum. Phosphate uptake experiments showed that maximal growth rates could be achieved with approximately 4% of the total phosphate-arsenate transport system. Organisms adapted to a range both of concentration of NaCl and of pH. Maximal affinity for phosphate occurred at pH 4 and at low concentrations of NaCl; however, V(max) for phosphate transport was little affected. Maximal specific growth rates on minimal medium were consistent in batch culture but gradually increased to the much higher rates found with yeast extract media when the population was subjected to long-term continuous culture with gradually increasing dilution rates. Phosphate initial uptake rates that were in agreement with the steady-state flux in continuous culture were obtained by using organisms and medium directly from continuous culture. This procedure resulted in rates about 500 times greater than one in which harvested batch-grown cells were used. Discrepancies between values found and those reported in the literature for other organisms were even larger. Growth could not be sustained below a threshold phosphate concentration of 3.4 nm. Such thresholds are explained in terms of a system where growth rate is set by intracellular nutrient concentrations. Threshold concentrations occur in response to nutrient sinks not related to growth, such as efflux and endogenous metabolism. Equations are presented for evaluation of growth rate-limiting substrate concentrations in the presence of background substrate and for evaluating low inhibitor concentration inhibition mechanisms by substrate prevention of inhibitor flux.

Arsenic↗
PubMed1973

Unusual arsenate poisoning of the F pili of Escherichia coli.

The arsenate poisoning of R17 phage eclipse in Escherichia coli cultures grown in glycerol-containing medium has been found to be mediated by a dramatic loss in cell-associated F pili. Poisoning was very rapid and was nearly complete within 3 min at 37 C. The loss of pili was reflected by a 90% reduction in the ability of these cells to attach ribonucleic acid phage and by a reduction in the pili-per-cell ratio from 1.36 to 0.04 as determined by electron microscopy. Neither the integrity of the pilus per se nor the attachment process was affected by arsenate, for cell-free pili treated with arsenate retained the ability to attach phage. The arsenate effect on F piliation could be reversed readily without any loss in cell viability. This restoration of pili occurred under conditions of inhibited protein synthesis, implying that pools of pili protein exist in cells. In contrast to this phenomenon, cells grown in glucose-containing media were mainly resistant to arsenate poisoning as determined by phage attachment and the number of pili per cell. These results implied that arsenate poisons the ability of cells to synthesize and maintain F pili under certain specific conditions. The possible mechanism of this poisoning is discussed.

Anaerobiosis↗
PubMed1983

Intracellular interaction and metabolic fate of arsenite and arsenate in mice and rabbits.

In vitro incubation of [74As]arsenite, -arsenate or -dimethylarsinic acid (DMA, the main metabolite of inorganic arsenic) with liver, lung and kidney homogenate of mice and rabbits showed that arsenite is the main form of arsenic bound to tissues. Injection of arsenite in mice and rabbits (0.04 mg As/kg body wt.) caused higher concentration of arsenic in the liver and the lungs than did the same dose of arsenate. This was less marked in the mice than in the rabbits, mainly due to the faster methylation to DMA. The relatively high degree of binding of arsenic to tissue constituents which also followed injection of arsenate may be explained by in vivo reduction to arsenite. The similar binding pattern after exposure to arsenite and arsenate indicates further that one and the same form of arsenic, arsenite, is retained independent of the form of exposure to inorganic arsenic. In contrast to the liver and lungs the kidneys showed a higher retention of arsenic after injection of arsenate than after injection of arsenite. Following injection of [74As]DMA in the animals excretion was essentially completed within 24 h, indicating low affinity for the tissues in vivo.

Animals↗
PubMed1985

Constant rate exposure of pregnant hamsters to arsenate during early gestation.

We have examined the teratogenic and embryotoxic effects of constant-rate exposure of pregnant hamsters to arsenate by means of subcutaneous implants of osmotic minipumps. Different total exposure regimens were established by varying the duration of minipump implants and by varying the concentration of arsenate in the minipumps. Dams were killed on Day 13 of pregnancy, 5 days after the critical stage of organogenesis. Numbers of resorptions, dead fetuses, and living fetuses were obtained. Fetal weights, crown-rump lengths, and the incidence of malformations were recorded. Control animals were treated identically with minipumps containing demineralized water. The percentage of malformations per litter, a direct measure of teratogenesis, was dependent only upon the concentration of arsenate in the minipumps. The minimum teratogenic response was achieved with a dose of 70 mumol/kg dam/24 hr during the critical stages of organogenesis. The embryotoxic (fetotoxic) indicators, fetal weight and crown-rump length, decreased with increases in exposure time and with increased concentrations of arsenate. The resorption rate also depended directly upon duration of exposure and concentration of arsenate in the minipump.

Abnormalities, Drug-Induced↗
PubMed1983

DNA homology between the arsenate resistance plasmid pSX267 from Staphylococcus xylosus and the penicillinase plasmid pI258 from Staphylococcus aureus.

A 29.5-kb plasmid, pSX267, from Staphylococcus xylosus DSM 20267 was found to code for arsenate, arsenite, and antimony (III) resistance. The isolated plasmid was transformed into S. aureus, where the same resistances were expressed. It was of special interest to see whether pSX267 showed any DNA sequence homology with the well-studied penicillinase plasmid from S. aureus pI258, also conferring arsenate, arsenite, and antimony III resistance. By the use of the Southern blotting technique, it was found that DNA sequence homology exists in the region of arsenate, arsenite, and antimony resistance, in addition to the region where the origin of replication, the incompatibility, and the replication A function were mapped on pI258. This finding was confirmed by electron microscope heteroduplex analysis, which allowed a correlation between the genetic and physical maps of pI258 and pSX267. Duplex DNA was formed at the arsenate operon of pI258, with a length of 2.6 kb, and at the incompatibility and replication A region, comprising a length of 2.5 kb. Adjacent to this latter region, two small regions of DNA homology were present, with lengths of 0.2 and 0.27 kb. Both plasmids share approximately 20% DNA sequence homology. The DNA homology of the arsenate, arsenite, and antimony III resistance coding regions between pI258 and pSX267 indicate that these plasmid-determined resistance markers are highly conserved and distributed among different staphylococcal species.

Antimony↗
PubMed2004

Mouse skin tumor promotion by sodium arsenate is associated with enhanced PCNA expression.

Drinking water contamination by arsenicals remains a major public health problem in many parts of the world more particularly in India and Bangladesh. Despite arsenic being a health hazard and implicated in human carcinogenesis, the experimental evidence available is much limited even now and the mechanisms involved during carcinogenesis and tumor promotions are not clear. Accordingly, in this study, we have studied the tumor promoter effects of sodium arsenate on mouse skin tumor promoter model system using 9,10-dimethyl-1,2-benzanthracene (DMBA) as a initiating carcinogen. Our studies showed development of papillomas on mice skin treated with only DMBA. However, mice treated with DMBA on skin and administered arsenate (As) in drinking water showed development of well differentiated squamous cell carcinomas. Further, both by immunohistochemistry and western blotting analysis studies higher levels of proliferating cell nuclear antigen (PCNA) was observed in mice treated with DMBA plus arsenate compared to only DMBA treated group. PCNA is known to be associated with S phase and DNA replication of the cell cycle. The plain controls and arsenate controls did not show significant difference either in tumor development or in PCNA levels. The present study demonstrates mouse skin tumor promoting effect of arsenate which seems to be associated with abnormal cell proliferation as indicated by higher levels of PCNA expression.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2006

Uptake, accumulation and depuration of sodium perchlorate and sodium arsenate in zebrafish (Danio rerio).

In toxicokinetics studies, interactions between chemicals in mixtures has been largely neglected. This study examines a mixture of perchlorate and arsenate because (1) they have the potential to co-occur in contaminated aquatic habitats, and (2) a previous study by the authors found possible toxicological interactive effects. In the present study, zebrafish (Danio rerio) were exposed to two concentrations of sodium perchlorate (10 and 100 mg l(-1)), sodium arsenate (1 and 10 mg l(-1)), and the mixture-sodium perchlorate+sodium arsenate (10+1 mg l(-1) and 100+10 mg l(-1) Na(2)HAsO(4)-high mixture) for 90 d. Their uptake and accumulation by zebrafish was evaluated at 10, 30, 60, and 90 d. In addition, depuration was examined at 1, 3, and 5d after cessation of the exposure. The uptake of either chemical was concentration-dependent, with significantly higher uptake at high concentrations at either exposure interval. In contrast, there was no significant difference in whole body residue between single chemicals and the corresponding mixture except for 100 mg l(-1) sodium arsenate at 90 d. However, there was increasing accumulation over time at the high concentration of either chemical alone and their mixture, and this increasing trend was more pronounced in the single chemical exposures than in the mixture. At the concentrations tested in the current study, both chemicals reduced the uptake but enhanced the depuration of the other chemical from the zebrafish. This study represents the first examination of the interaction of two anions-perchlorate and arsenate with respect to toxicokinetics.

Animals↗
PubMed2005

Adsorption of arsenate on soils. Part 2: modeling the relationship between adsorption capacity and soil physiochemical properties using 16 Chinese soils.

An attempt has been made to elucidate the effects of soil properties on arsenate adsorption by modeling the relationships between adsorption capacity and the properties of 16 Chinese soils. The model produced was validated against three Australian and three American soils. The results showed that nearly 93.8% of the variability in arsenate adsorption on the low-energy surface could be described by citrate-dithionite extractable Fe (Fe(CD)), clay content, organic matter content (OM) and dissolved organic carbon (DOC); nearly 87.6% of the variability in arsenate adsorption on the high-energy surface could be described by Fe(CD), DOC and total arsenic in soils. Fe(CD) exhibited the most important positive influence on arsenate adsorption. Oxalate extractable Al (Al(OX)), citrate-dithionite extractable Al (Al(CD)), extractable P and soil pH appeared relatively unimportant for adsorption of arsenate by soils.

Adsorption↗
PubMed2005

Enumeration and characterization of culturable arsenate resistant bacteria in a large estuary.

Arsenic is a toxic element that exists in two major inorganic forms, arsenate and arsenite. A number of bacteria have been shown to resist arsenic exposure, and even more bacteria appear to possess the genes for arsenic resistance. In this study, the numbers of culturable arsenate-resistant bacteria present in water at three coastal sites in the Lake Pontchartrain estuary, Louisiana, was determined. Despite insignificant (less than 1.33 microM) levels of arsenic in this system, 20-50% of the viable count of bacteria showed appreciable arsenate resistance, suggesting that arsenic-resistant bacteria are common and widespread. A diverse array of arsenate-resistant isolates was obtained, with 16S rRNA sequence analysis indicating 37 different bacterial strains, representing six major bacterial groups. Many of these isolates were affiliated with groups of bacteria that have been poorly characterized in terms of arsenic resistance, such as the Betaproteobacteria or Flavobacteria. Some isolates were capable of tolerating very high (> 100 mM) levels of arsenate, although arsenite resistance was generally much lower. The results suggest that arsenic-resistant bacteria are common, even in environments with insignificant arsenic contamination, and that many different groups of aquatic bacteria show appreciable arsenic resistance.

Arsenates↗