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PubMedDate not supplied

Total arsenic in foods after sequential wet digestion, dry ashing, coprecipitation with ammonium pyrrolidine dithiocarbamate, and graphite-furnace atomic absorption spectrometry.

A graphite-furnace atomic absorption (GFAAS) method is described for determining total arsenic (organic and inorganic compounds) in foods. Samples ranging from 1 to 40 g (depending on moisture content) were digested with HNO3 and dry-ashed at 500 degrees C overnight after addition of MgO. After dissolution in HCl, the arsenic was reduced with iodide and ascorbic acid and precipitated with ammonium pyrrolidine dithiocarbamate (APDC) in the presence of nickel carrier. Precipitates were collected on 0.3 micron cellulose acetate filters and dissolved in 10% HNO3 containing modifier. Ba(NO3)2 was added to remove a sulfate interference resulting from decomposition of APDC. Arsenic was determined using GFAAS. Accuracy of the method was good for 7 U.S. National Bureau of Standards (NBS) Standard Reference Materials and 3 National Research Council of Canada (NRCC) round-robin samples. Recovery of arsenic(V) from foods averaged 99.2% for peak heights and 97.1% for peak areas, with relative standard deviations (RSD) of 2.2% for peak heights and 3.3% for peak areas for all NBS and NRCC materials. Detection limit of the method was ca 10 ng arsenic.

Arsenic↗
PubMed2005

Metabolites produced by nitrogen-fixing Nostoc species.

This paper provides a comprehensive overview of metabolites, including lipids and lipid-like compounds, boron-containing macrocycles, arsenolipids, oligopeptides and amino acid derivatives, produced by cyanobacteria of the genus Nostoc.

Amino Acids↗
PubMed2003

Active arsenic species produced by GSH-dependent reduction of dimethylarsinic acid cause micronuclei formation in peripheral reticulocytes of mice.

Dimethylarsine and trivalent dimethylated arsenic, metabolites of inorganic arsenics, have received considerable attention in current research because of their biological activities. We attempted to determine the appearance of micronucleated reticulocytes (MNRETs) in mouse peripheral blood following intraperitoneal administration of dimethylarsinous iodide (DMI) and trimethylarsine (TMA), model compounds of trivalent dimethylated arsenic and dimethylarsine, respectively. A significant increase in the number of MNRETs was observed with TMA, but not with DMI. Furthermore, MNRETs only appeared with 10.6 mg/kg of dimethylarsinic acid (DMA) following its co-injection with reduced glutathione (GSH). These results suggest that micronucleus formation may need further metabolic reduction of trivalent dimethylated arsenic, i.e. the production of dimethylarsine, by an excess amount of GSH. Meanwhile, the increase in MNRETs by administration of arsenite at 7.6 mg/kg, an equivalent dose to DMA as As, was remarkably diminished by co-administration with GSH. These results indicate that GSH plays an important role in the genotoxic process of arsenics, particularly by dimethylated arsenic.

Animals↗
PubMed2001

Biosynthesis and release of methylarsenic compounds during the growth of freshwater algae.

Arsenic transformations by freshwater algae have been studied under laboratory conditions. By the use of a new analytical method, we identified methylarsenic(III) species in the growth medium of green-alga Closterium aciculare incubated under axenic conditions. The arsenate concentration in the experimental medium began to decrease just after inoculation, and the levels of arsenite and methylarsenicals increased with the growth of C. aciculare. Initially, most of the arsenate was converted into arsenite, which peaked in concentration during the exponential phase. Methylarsenicals accumulated rapidly in the stationary phase. DMAA(V) production was enhanced when the ratio of phosphate to arsenate decreased in the culture medium. The levels of DMAA(V) increased continuously toward the end of the experiment. On the other hand, methylarsenic(III) species remained relatively steady during the stationary phase. Methylarsenic(III) species accounted for 0-35% of methylarsenicals. These results suggest that arsenite and methylarsenicals (containing methylarsenic(III) species) are supplied by phytoplankton, and serve as evidence of the origin of methylarsenic(III) species in natural waters.

Arsenates↗
PubMed2006

Anti-proliferative effects of novel glyco-lipid-arsenicals (III) on MCF-7 human breast cancer cells.

Arsenic trioxide appears to be effective in the treatment of pro-myelocytic leukaemia. The substituted phenylarsen(III)oxides are highly polar, they have a high tendency to undergo oxidation to As (V) and to form oligomers, to prevent this we protected the As-(OH)(2) group as cyclic dithiaarsanes. To increase the compound's biological stability and passive diffusion we conjugated the compound of interest with lipoamino acids (Laas). Alternatively, we further conjugated the dithiaarsane derivative with a carbohydrate to utilize active transport systems and to target compound. We investigated two novel glyco-lipid arsenicals (III) (compounds 9 and 11) for their ability to initiate MCF-7 breast cancer cell death and characterized the mechanism by which death was initiated. A significant decrease in MCF-7 cell proliferation was observed using 1 microM and 10 microM compound (11) and 10 microM of compound (9). Treatment with compound (11) triggered apoptosis of MFC-7 cells while compound (9) induced inhibition of cellular proliferation was not via rapid induction of apoptosis and more likely reflected necrosis and/or alterations in the cell cycle. Differences in the anti-proliferative potency of the two compounds indicate that structural modifications influence effectiveness.

Antineoplastic Agents↗
PubMed1991

Substituent effects on the binding constants of arsenical-dithiol adducts.

Proton nuclear magnetic resonance spectroscopy (1H NMR) was used to determine the relative binding constants for several arsenical-dithiol adducts. The compounds investigated were 2,3-dimercaptopropanol (British anti-lewisite; BAL), 1,2-ethane dithiol (ET), and 1,2-propane dithiol (PDT). It was found that PDT has a significantly higher affinity than ET or BAL for phenyldichloroarsine (PDA) in methanol.

Arsenicals↗
PubMed1972

Antigen recognition and the immune response. Humoral and cellular immune responses to small mono- and bifunctional antigen molecules.

L-Tyrosine azobenzene-p-arsonate (RAT) induced cellular immunity without antibody production in guinea pigs. Bifunctional antigens were prepared consisting of one RAT carrier moiety linked either directly to a dinitrophenyl (DNP) haptenic determinant or through one or more 6-amino-caproyl (SAC) spacers. Each SAC unit has an extended span of 8 A. Guinea pigs immunized with these conjugates developed cellular immunity directed against the RAT determinant and antibody specific for the DNP determinant. The anti-DNP response was the same with one or three SAC spacers, but was significantly weaker when the two determinants were joined without a spacer. Animals immunized with either DNP-SAC-TYR or DNP-TYR developed neither cellular nor humoral immunity. Prior immunization with RAT potentiated the secondary anti-hapten response to DNP-SAC-RAT. Modification of RAT at either the arsonate or tyrosine positions showed that other charged groups (sulfonate and trimethylammonium) could substitute for arsonate without loss of immunogenicity. Removal of either the amino or carboxyl group from the side chain of tyrosine did not abolish immunogenicity, but immunogenicity was lost upon removal of both. Immunization with symmetrical bifunctional RAT-(SAC)(n)-RAT and cyclo-(L-RAT-D-RAT) antigens led to cellular immunity but no anti-arsonate antibody, suggesting a barrier to "self-help." These compounds were also ineffective in inducing a secondary anti-arsonate response in animals primed with arsonate-BSA conjugates and RAT.

Animals↗
PubMed1990

A rapid microassay for hemolytic antibody--its application to immunotoxicological study.

A rapid microassay for hemolytic antibody using an automatic spectrophotometer was developed. This microassay was parallel to hemolytic plaque forming cell (PFC) assay most commonly used to detect antibody formation. The former had more advantages than the latter did. The data obtained using arsenic and some metallic compounds as immunomodifiers suggested that this microassay was suitable for the screening of immunomodifiers in immunotoxicological and immunopharmacological studies which deal with a large number of samples within limited time.

Animals↗
PubMed1980

Distribution of 23 elements in the kidney, liver and lungs of workers from a smeltery and refinery in North Sweden exposed to a number of elements and of a control group.

The levels of antimony, arsenic, cadmium, caesium, chromium, cobalt, copper, gold, iron, lanthanum, lead, manganese, mercury, molybdenum, phosphorus, rubidium, scandium, selenium, silver, tellurium, tin, tungsten and zinc in the kidney, liver and lungs of autopsy specimens from exposed workers in North Sweden, as well as from a control group, have been assayed quantitatively. The workers had been exposed to several elements and their compounds, e.g. lead, mercury, arsenic and cadmium, for long periods in arsenic, lead or selenium plants and in a lead or copper smelter. The chemical analysis was by neutron activation analysis and atomic absorption spectrophotometry. Median levels of antimony, arsenic, cadmium, chromium cobalt, lanthanum, lead or selenium in kidney, liver or lungs in the exposed worker group were found to be about 2 to 16 times as great as the corresponding levels for the control group. Long biological half-life values were observed for these elements, especially in lung tissue.

Aged↗
PubMed2004

Cellular glutathione prevents cytolethality of monomethylarsonic acid.

Inorganic arsenicals are clearly toxicants and carcinogens in humans. In mammals, including humans, inorganic arsenic often undergoes methylation, forming compounds such as monomethylarsonic acid (MMAs(V)) and dimethylarsinic acid (DMAs(V)). However, much less information is available on the in vitro toxic potential or mechanisms of these methylated arsenicals, especially MMAs(V). We studied the molecular mechanisms of in vitro cytolethality of MMAs(V) using a rat liver epithelial cell line (TRL 1215). MMAs(V) was not cytotoxic in TRL 1215 cells even at concentrations exceeding 10 mM, but it became weakly cytotoxic and induced both necrotic and apoptotic cell death when cellular reduced glutathione (GSH) was depleted with the glutathione synthase inhibitor, l-buthionine-[S,R]-sulfoximine (BSO), or the glutathione reductase inhibitor, carmustine. Similar results were observed in the other mammalian cells, such as human skin TIG-112 cells, chimpanzee skin CRT-1609 cells, and mouse metallothionein (MT) positive and MT negative embryonic cells. Ethacrynic acid (EA), an inhibitor of glutathione S-transferase (GST) that catalyses GSH-substrate conjugation, also enhanced the cytolethality of MMAs(V), but aminooxyacetic acid (AOAA), an inhibitor of beta-lyase that catalyses the final breakdown of GSH-substrate conjugates, had no effect. Both the cellular GSH levels and the cellular GST activity were increased by the exposure to MMAs(V) in TRL 1215 cells. On the other hand, the addition of exogenous extracellular GSH enhanced the cytolethality of MMAs(V), although cellular GSH levels actually prevented the cytolethality of combined MMAs(V) and exogenous GSH. These findings indicate that human arsenic metabolite MMAs(V) is not a highly toxic compound in mammalian cells, and the level of cellular GSH is critical to its eventual toxic effects.

Aminooxyacetic Acid↗
PubMed1989

Accumulation of arsenic in yelloweye mullet (Aldrichetta forsteri) following oral administration of organoarsenic compounds and arsenate.

Groups of yelloweye mullet (Aldrichetta forsteri) were maintained for several weeks on diets containing one of a range of organoarsenic compounds (arsenobetaine, arsenocholine, 2-dimethylarsinylethanol, 2-dimethylarsinylacetic acid, 2-dimethylarsinothioylethanol) or arsenate. Fish fed 2-dimethylarsinylethanol, 2-dimethylarsinylacetic acid or 2-dimethylarsinothioylethanol showed no increase in arsenic concentrations in their muscle tissue, while fish fed arsenate showed small increases. The two groups of fish which received either arsenobetaine or arsenocholine had greatly elevated arsenic concentrations in their muscle tissue resulting from an estimated approximately 40% retention of ingested arsenic. Examination of the form of arsenic accumulated by fish fed arsenocholine showed that most of the arsenic (89%) was accumulated as arsenobetaine.

Administration, Oral↗
PubMed1995

Toxic gas generation from plastic mattresses and sudden infant death syndrome.

Microbial generation of toxic gases from antimony, arsenic, or phosphorus in compounds used as fire retardants in cot mattresses has been proposed as a cause of sudden infant death. To test this hypothesis, 23 polyvinyl chloride mattress samples from cot death cases were incubated on malt agar plates until good microbial growth was obtained. Silver nitrate and mercuric chloride test papers were then inserted and the colour reactions recorded. The predominant organism, recovered from all mattresses tested, was not, as claimed in earlier work, the fungus Scopulariopsis brevicaulis, but a mix of common environmental Bacillus spp. Test paper colour changes occurred whenever bacterial growth was present, but these reactions also occurred in control tests in which no mattress material was present on the plates. Chemical and instrumental analyses of exposed test papers showed that the colour reactions were not due to deposits of antimony, arsenic, or phosphorus. Our findings do not support the hypothesis that toxic gases derived from antimony, arsenic, or phosphorus are a cause of sudden infant death. More sulphur was found in test papers exposed in plates containing bacterial growth than in those without such growth. This result suggests that the test paper reactions were due to the generation of sulphur-containing compounds during bacterial growth on the agar medium.

Bacillus↗
PubMedDate not supplied

Morphological changes of labyrinthine blood vessels following metal poisoning.

Metal intoxication (mercury and arsenic) in guinea pigs may cause damage to labyrinthine blood vessels by swelling of the endothelial cells, mitochondrial disintegration and sometimes protrusion of endothelial cell cytoplasm herniating into the blood vessel lumen. Chronic mercury intoxication resulted in distorted endothelial cells with an increase in the density of their cytoplasm. An altered vascular permeability is likely to occur as the result of the morphological changes.

Aniline Compounds↗
PubMed2004

Toxicity of indium arsenide, gallium arsenide, and aluminium gallium arsenide.

Gallium arsenide (GaAs), indium arsenide (InAs), and aluminium gallium arsenide (AlGaAs) are semiconductor applications. Although the increased use of these materials has raised concerns about occupational exposure to them, there is little information regarding the adverse health effects to workers arising from exposure to these particles. However, available data indicate these semiconductor materials can be toxic in animals. Although acute and chronic toxicity of the lung, reproductive organs, and kidney are associated with exposure to these semiconductor materials, in particular, chronic toxicity should pay much attention owing to low solubility of these materials. Between InAs, GaAs, and AlGaAs, InAs was the most toxic material to the lung followed by GaAs and AlGaAs when given intratracheally. This was probably due to difference in the toxicity of the counter-element of arsenic in semiconductor materials, such as indium, gallium, or aluminium, and not arsenic itself. It appeared that indium, gallium, or aluminium was toxic when released from the particles, though the physical character of the particles also contributes to toxic effect. Although there is no evidence of the carcinogenicity of InAs or AlGaAs, GaAs and InP, which are semiconductor materials, showed the clear evidence of carcinogenic potential. It is necessary to pay much greater attention to the human exposure of semiconductor materials.

Aluminum Compounds↗