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PubMed1980

Absence of arsenite mutagenicity in E coli and Chinese hamster cells.

Because exposure to compounds of arsenic has been implicated as a cause of cancer, an investigation of the mutagenicity of sodium aresenite in E coli and in Chinese hamster cells was performed. In the E coli system, Trp + revertants were not induced by arsenite in a variety of experimental protocols including spot tests, treat and plate protocols, and fluctuation tests. The mutator effect of a tif-1 strain was partially blocked by arsenite. Arsenite did not cause the induction of lambda prophage. In Chinese hamster cells, arsenite did not induce ouabain-resistant mutants or thioguanine-resistant mutants. We conclude that arsenite is not mutagenic to E coli or to Chinese hamster cells. When added to the plating medium, arsenite can act as an anti-mutagen by inhibition of induction of the error-prone SOS repair system in E coli.

Animals↗
PubMed2002

An investigation of the chemical stability of arsenosugars in simulated gastric juice and acidic environments using IC-ICP-MS and IC-ESI-MS/MS.

A more quantitative extraction of arsenic-containing compounds from seafood matrices is essential in developing better dietary exposure estimates. More quantitative extraction often implies a more chemically aggressive set of extraction conditions. However, these conditions may result in undesirable chemical changes in the native arsenicals which may further complicate the toxicological risk assessment. This balance between quantitative extraction and species-specific integrity may be best addressed by using simulated gastric juice as an extraction solvent to mimic 'bioavailability'. This, conceptually, should extract the bioavailable fraction and induce any chemical changes that would occur because of ingestion. The most chemically labile species associated with seafood are thought to be the arsenosugars and for this reason their chemical stability is investigated in this study. Four arsenosugars (3-[5'-deoxy-5'-(dimethylarsinoyl)-beta-ribofuranosyloxy]-2-hydroxypropylene glycol, As(328); 3-[5'-deoxy-5'-(dimethylarsinoyl)-beta-ribofuranosyloxy]-2-hydroxypropanesulfonic acid, As(392); 3-[5'-deoxy-5'-(dimethylarsinoyl)-beta-ribofuranosyloxyl-2-hydroxypropyl hydrogen sulfate, As(408); and 3-[5'-deoxy-5'-(dimethylarsinoyl)-beta-ribofuranosyloxy]-2-hydroxypropyl-2,3-hydroxypropyl phosphate, As(482)) were isolated from seaweed extracts and subjected to simulated gastric juice and acidic conditions which mimic the stomach's pH of 1.1. Three acid solutions were used to test the chemical stability of the arsenosugars: simulated gastric juice, 78 mM nitric acid and 78 mM hydrochloric acid. The composition of the solutions was monitored over time (up to 48 h) using IC-ICP-MS for detection. The arsenosugars were found to degrade at the rate of 1.4% per h at 38 degrees C and 12.2% per h at 60 degrees C. The plots of percent conversion versus time were found to be independent of the starting arsenosugar and all had r2 values of greater than 0.97. A single common degradation product was observed in all the stability studies. A mass balance between the starting arsenosugar (As(392), As(408) and As(482)) and the degradation product was conducted with each set of experiments. This mass balance indicated that the degradation process did not produce any unchromatographable species. This degradation product was tentatively identified as As(254) as determined by ESI-MS/MS spectral data. An acid hydrolysis mechanism was proposed for the formation of As(254) from each of the native arsenosugars by hydrolysis at the C-1 carbon on the ribose ring.

Animals↗
PubMed2000

[Studies on fluorimetric method for the determination of trace arsenic (III) with 2',7'-dichlorofluorescein].

A rapid, simple and sensitive fluorimetric new method has been developed for the determination of trace amounts of arsenic (III) with 2',7'-dichlorofluorescein as fluorogenic reagent (lambda ex = 508 nm, lambda em = 524 nm) at pH 5.5-7.5. In a neutral medium, I2 reacts with 2',7'-dichlorofluoresce to produce a non-fluorescence compound. If arsenic (III) is present, the fluorescence intensity of the solution increases with the increasing concentration of As3+ when appropriate amounts of I2 and 2',7'-dichlorofluorescein are added. A linear calibration curve was obtained in the range of 1.0-80.0 micrograms.L-1, the detection limit is 1.0 microgram.L-1. It has been applied to the determination of As3+ in the waste water and river water with satisfactory results.

Arsenic↗
PubMed2006

Interaction of tin(II) and arsenic(III) with DNA at the nanostructure film modified electrodes.

Biosensors based on DNA and DNA-carbon nanotubes film immobilized at the surface of a screen-printed carbon electrode were used for simple in vitro tests of chemical toxicity. The damage to DNA caused by tin(II) and arsenic(III) compounds as components of specific reaction media was evaluated by means of an electrochemical DNA marker, [Co(phen)3](3+), as the portion of original dsDNA which survives an incubation of the biosensor in the cleavage medium. The results were confirmed by the electrically heated electrode and by the measurement of the DNA guanine moiety signal.

Arsenic↗
PubMed1984

Arsenic-sulfur amino acid interactions in the chick.

Experiments were conducted with growing crossbred chicks to determine the reasons why cysteine exacerbates roxarsone (3-nitro-4-hydroxyphenylarsonic acid) toxicity. A fortified corn-soybean meal diet that met or exceeded all nutrient requirements of the young chick was fed. While cysteine enhanced roxarsone toxicity, it had little effect on the toxicity of the inorganic arsenicals As2O3 and As2O5. The toxicity of another pentavalent organic arsenical, phenylarsonic acid, was also exacerbated by cysteine. In contrast, the growth-depression resulting from feeding the trivalent form of phenylarsonic acid, i.e., phenylarsine oxide, was not affected by dietary addition of cysteine. Supplementation of the diet with cystine, methionine or K2SO4 did not exacerbate roxarsone toxicity. Reduced glutathione (GSH), however, slightly increased the gain/feed depression resulting from feeding 300 mg roxarsone/kg diet. When injected ip 1) roxarsone and cysteine, or 2) roxarsone and ascorbic acid killed 100 or 60% of the birds, respectively, within 48 h postinjection. Few (6.7%) deaths resulted from ip injections of the same level of roxarsone alone. Therefore, the potentiation of toxicity requires pentavalent organic arsenicals and compounds that can act as reducing agents. We concluded that cysteine exacerbates roxarsone toxicity by reducing it to the more toxic trivalent state.

Amino Acids, Sulfur↗
PubMed1996

Dietary exposures to selected metals and pesticides.

Average daily dietary exposures to 11 contaminants were estimated for approximately 120,000 U.S. adults by combining data on annual diet, as measured by a food frequency questionnaire, with contaminant residue data for table-ready foods that were collected as part of the annual U.S. Food and Drug Administration Total Diet Study. The contaminants included in the analysis were four heavy metals (arsenic, cadmium, lead, mercury), three organophosphate pesticides (chlorpyrifos, diazinon, malathion), and four organochlorine pesticides (dieldrin, p,p'-DDE, lindane, heptachlor epoxide). Dietary exposures to these contaminants were highly variable among individuals, spanning two to three orders of magnitude. Intraindividual exposures to the metals, organophosphates, and organochlorines were estimated to be strongly correlated; Pearson's correlation coefficients ranged from 0.28 for lindane:dieldrin to 0.84 for lead:mercury. For some of the compounds (e.g., arsenic and dieldrin), a substantial fraction of the population was estimated to have dietary intakes in excess of health-based standards established by the EPA. Before use for risk assessment or epidemiologic purposes, however, the validity of the exposure estimates must be evaluated by comparison with biological indicators of chronic exposure. Because of their low detection rate in table-ready foods, the estimated distributions of exposures for dieldrin, p,p'-DDE, heptachlor epoxide, lindane, diazinon, and chlorpyrifos were found to be sensitive to assumed values for nondetect samples. Reliable estimates of the population distribution of dietary exposures to most other contaminants cannot be made currently, due to their low rate of detection in table-ready foods. Monitoring programs that use more sensitive study designs and population-based assessments for other subpopulations should be a priority for future research.

Adult↗
PubMed2003

Gas-phase chemistry of ethynylamine, -phosphine and -arsine. Structure and stability of their Cu+ and Ni+ complexes.

The Cu+ and Ni+ binding energies of ethynylamine, ethynylphosphine and ethynylarsine have been calculated at the B3LYP/6-311 + G(2df,2p)//B3LYP/6-311G(d,p) level of theory. Significant differences between nitrogen-containing and phosphorus- or arsenic-containing compounds have been found regarding structural effects upon metal cation association. While for ethynylamine the global minimum of the potential energy surface corresponds to the complex in which the metal cation binds to the beta-carbon, for ethynylphosphine the most favourable process corresponds to phosphorus attachment. For ethynylarsine, the conventional pi-complex is the most stable one. This behavior resembles that found for the corresponding vinyl analogues, with the only exception being the arsenic derivative. The calculated Cu+ and Ni+ binding energies for attachment to the heteroatom follow a different trend, P > As > N, to that predicted for the corresponding proton affinities, P > N > As. Cu+ and Ni+ binding energies are almost identical when the metal cation binds to the heteroatom. However, Ni+ binding energies are slightly larger than Cu+ binding energies when the metal cation interacts with the C identical to C bond.

Journal Article↗
PubMed1993

Arsenic in the sera of gallium arsenide-exposed mice inhibits bacterial growth and increases host resistance.

The objective of the present investigations was to evaluate whether the presence of gallium arsenide (GaAs) in the sera of exposed mice was sufficient to retard bacterial growth. Host resistance studies demonstrated that exposure of GaAs (50-200 mg/kg) produced an increased resistance to Streptococcus pneumoniae and Listeria monocytogenes (50-100 mg/kg GaAs) when microbial challenge occurred 24 hr after exposure. In contrast, exposed mice exhibited a profound and dose-related decrease in resistance to the B16F10 melanoma. Serial dilutions of GaAs (0.039-5 mg/ml) were added to BHI broth and cultures were innoculated with either S. pneumoniae or L. monocytogenes. GaAs slowed the growth of both organisms with a minimal inhibitory concentration (MIC) of 0.625 mg/ml. Sera from mice euthanized at various time intervals after exposure to vehicle (0.05% Tween 80 in saline) or GaAs (200 mg/kg) was also capable of retarding the growth of both organisms with the maximal inhibition noted for euthanization 24 hr after exposure. However, sera from GaAs-exposed mice (24 hr after exposure) was incapable of slowing the growth of the B16F10 melanoma. Addition of the arsenic-binding compound meso-2,3-dimercaptosuccinic acid (100 microM) to sera from mice exposed to GaAs followed by innoculation with L. monocytogenes resulted in growth of this organism, which was comparable to growth observed in vehicle cultures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Arsenic toxicity in Hawaii: a case report and review.

As mentioned at the beginning of this article, many questions were raised in our one particular case including the problem of verifying true arsenic toxicity and in determining the source of the exposure. In our case, there was a markedly elevated concentration of arsenic in samples of pubic hair and in the sample of urine. While arsenic toxicity can present with GI symptoms, we felt that in this particular case the association of the abdominal pain with arsenic toxicity was unlikely. For one, the patient's symptoms persisted despite apparent adequate treatment for arsenic toxicity. Also, the usual symptom of chronic arsenic toxicity is peripheral neuropathy (which was not documented in our case) and not abdominal pain. After the exhaustive diagnostic workup, we felt that this patient had irritable bowel syndrome and that the discovery of arsenic toxicity was serendipitous. In regards to the etiology of the toxicity, the patient's occupation involved working in the construction industry for a number of years. He indicated a definite exposure to termite-treated wood throughout that period. Wood for building houses, etc. is commonly pressure-treated with an arsenic-based compound; therefore, this source of occupational exposure appears to be a likely one. Another remotely possible source was the ingestion of contaminated illicit drugs. Cases of the use of illicit drugs laced with various toxic agents such as cyanide and strychnine have been reported. Although our patient required analgesics not commensurate with his symptoms, he categorically denied any use of "street" drugs. The random urine drug screen for such was negative.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Syntheses and structures of heterobicyclic bis(tert-butylamido)cyclodiphosph(III)azane compounds having phosphorus(III) and arsenic(III) centers.

Syntheses and single-crystal X-ray diffraction studies of heterobicyclic cyclodiphosphazanes having central phosphorus(III) and arsenic(III) atoms are described. Interaction of PCl3 or AsCl3 with cis-[(tBuNP)2(tBuNLixTHF)2] produced the isomorphous ([(tBuNP)2(tBuN)2]ECl); E = P(1), As(4), respectively. These Cs-symmetric molecules crystallize with two molecules in the monoclinic space group P2(1)/m. Unit cell dimensions of 1 are (293 K) a = 9.777(1) A, b = 11.745(1) A, c = 9.986(2) A, and beta = 97.44(1) degrees; those of 4 are (213 K) a = 9.688(3) A, b = 11.873(3) A, c = 9.975(3) A, and beta = 97.80(3) degrees. When ([(tBuNP)2(tBuN)2]PCl) was treated with NaN3 or LiN(SiMe3)2, ([(tBuNP)2(tBuN)2]PN3)(2) and ([(tBuNP)2(tBuN)2]PN(SiMe3)2)(3), respectively, were obtained. Compound 2 crystallizes in the monoclinic space group P2(1)/m and has until-cell dimensions (213 K) of a = 9496(7) A, b = 12455(7) A, c = 10043(6) A, and beta = 9723(4) degrees, Z = 2.

Journal Article↗
PubMed2004

Arsenic removal from groundwater by a newly developed adsorbent.

A novel adsorbent, which had been developed for phosphate adsorption, was adopted for arsenic removal from groundwater. Adsorption isotherm, pH dependence of the isotherm and adsorption rate were studied by batch method. Furthermore, by using a granular adsorbent of 1.8 mm diameter which is commercially available, lab-scale experiments of continuous adsorption treatment of actual groundwater containing arsenic at 50 mg m(-3) were conducted to examine the performance of the adsorbent. A large amount of arsenic, i.e., 10 g As kg(-1), was adsorbed at pH 7.0 and 10 mg As m(-3) in equilibrium concentration. It was only a 5% higher amount compared to conventional activated alumina. However, twice the bed volume, i.e., total volume of effluent divided by empty column volume, was achieved till breakthrough by using this novel adsorbent. This may be because the pH decrease, which enlarges apparent adsorption capacity of the adsorbent, is caused by a self-pH decrease function of the adsorbent. The self-pH decrease function must be delivered by dissociation of Al (III) aquoion. The proton release was clearly observed in batch experiments.

Adsorption↗
PubMed2001

[Kinetics of arsenic in human blood after a fish meal].

It is well known that fish contains high amounts of arsenic (As) compounds (mean values per wet weight [mg x kg-1] Ballin [1]: 41; Falconer et al. [2]: 14; Staveland et al. [3]: 5.2), which are mainly represented by organic As compounds, especially by arsenobetaine. It is generally assumed that arsenobetaine is rapidly eliminated via the urine and therefore seems to be non-toxic for humans. However, the kinetics of arsenobetaine in human blood are unknown to date. Therefore, the following experiments were performed: 14 women of 24 to 32 years of age voluntarily ingested 179 to 292 g of cooked plaice fillet containing 44 (minimum) to 276 (maximum) mg As x kg-1 dry weight. Hence, the volunteers ingested 2.5 (minimum) to 20 (maximum) mg As per person, equivalent to 0.04 to 0.35 mg As x kg-1 body weight. The element As was measured by atomic absorption spectrometry using the graphite furnace technique in order to detect the total amount of As including that of the stable arsenobetaine. In the blood, the highest As values of 55 +/- 5.8 micrograms x L-1 (median) were found 2 hours after fish ingestion. Subsequently the As concentrations declined reaching 16 +/- 0.69 micrograms x L-1 (median) 48 hours after fish ingestion. In respect of the As values in blood recorded between 2 and 10 hours after fish ingestion, rapid elimination could be observed leading to a half-life of 7.1 hours (first value) recorded by linear regression analysis. With regard to the As values in blood between 10 and 48 hours after fish ingestion, a lower elimination rate was estimated with a longer half-life of 63 hours (second value). The reason for this delayed elimination of As is not known. The results indicate that As mainly absorbed as arsenonetaine due to ingestion of fish is not eliminated as fast as had been expected on the basis of published data. As long as it is not known what happens to arsenobetaine remaining for longer periods in the blood with a half-life of 63 hours, caution is advised regarding the general opinion that arsenobetaine is rapidly eliminated and non-toxic for human consumption.

Adult↗
PubMed1987

Inhibition of O6-alkylguanine-DNA-alkyltransferase by metals.

The activity of the DNA-repair protein O6-alkylguanine-DNA-alkyltransferase was found to be strongly inhibited by a number of metal ions. Cd2+ was the most active followed by Cu2+, Hg2+, Zn2+ and Ag2. This inhibition is likely to result from the interaction of the metals with the cysteine-acceptor residue on the protein since the inhibition was reduced by increasing the concentration of dithiothreitol in the assay buffer. These results raise the possibility that exposure to Cd2+ could increase the mutagenicity and carcinogenicity of alkylating agents by retarding the rate of repair of alkylated DNA. However, other metals or metallic compounds which are known to be carcinogenic (such as compounds containing arsenic, lead, nickel or chromium) did not interfere with DNA repair by this protein.

Animals↗
PubMed2005

Theoretical study of aluminum arsenide clusters: equilibrium geometries and electronic structures of Al(n)As(n) (n=1-4).

The geometry, electronic configurations, harmonic vibrational frequencies and stability of the structural isomers of Al(n)As(n) clusters (n=1-4) have been investigated using density functional theory. For dimers and trimers, the lowest energy structures are planar cumulenic rings (IIs, VIs) with D(nh) symmetry. The caged structure with T(d) symmetry (IXs) lie lowest in energy among the tetramers. The AlAs bond dominates the structures for many isomers so that one preferred dissociation channel is loss of the AlAs monomer. The atomic charges, hybridization and chemical bonding in the different structures are also discussed. Comparisons with valence-isoelectronic Si(2n), Al(n)P(n) and Ga(n)As(n) clusters of same size, the properties of the aluminum arsenide clusters are analogous to those of their corresponding Al(n)P(n), Si(2n) counterparts. The results can explain the modification and refinement of Si phase in AlSi alloy in the molecular level.

Aluminum Compounds↗
PubMed2004

Pulsed optically detected NMR of single GaAs/AlGaAs quantum wells.

While nuclear magnetic resonance (NMR) is one of the most important experimental tools for the analysis of bulk materials, the low sensitivity of conventional NMR makes it unsuitable for the investigation of small structures. We introduce an experimental scheme that makes NMR spectra of single, nanometer-sized quantum wells possible with excellent sensitivity and selectivity while avoiding the spectral broadening associated with some alternative techniques. The scheme combines optical pumping and pulsed radiofrequency excitation of the nuclei with time-resolved detection of the free induction decay through the polarization of the photoluminescence.

Aluminum Compounds↗