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Mammals are able to convert inorganic arsenic to mono-, di-, and trimethylated metabolites. In previous studies we have shown that the trivalent organoarsenic compounds are more toxic than their inorganic counterparts and that the toxicity is associated with the cellular uptake of the arsenicals. In the present study, we investigated cyto-/genotoxic effects of the arsenic compounds arsenate [As(i)(V)], arsenite [As(i)(III)], monomethylarsonic acid [MMA(V)], monomethylarsonous acid [MMA(III)], dimethylarsinic acid [DMA(V)], dimethylarsinous acid [DMA(III)], and trimethylarsine oxide [TMAO(V)] after an extended exposure time (24 h) and compared the uptake capabilities of fibroblasts (CHO-9 cells: Chinese hamster ovary) used for genotoxicity studies, with those of hepatic cells (Hep G2: hepatoma cell-line). To find out whether the arsenic compounds are bound to membranes or if they are present in the cytosol, the amount of arsenic was measured in whole-cell extracts and in membrane-removed cell extracts by inductively coupled plasma-mass spectrometry (ICP-MS). In addition, we forced the cellular uptake of the arsenic compounds into CHO-9 cells by electroporation and measured the intracellular arsenic concentrations before and after this procedure. Our results show that organic and inorganic arsenicals are taken up to a higher degree by fibroblasts compared to hepatoma cells. The arsenic metabolite DMA(III) was the most membrane permeable species in both cell lines and induced strong genotoxic effects in CHO-9 cells after an exposure time of 24 h. The uptake of all other arsenic species was relatively low (<1% by Hep G2 and <4% by CHO cells), but was dose-dependent. Electroporation increased the intracellular arsenic levels as well as the number of induced MN in CHO-9 cells. With the exception of As(i)(III) and DMA(III) in CHO-9 cells, the tested arsenic compounds were not bound to cell membranes, but were present in the cytosol. This may indicate the existence of DMA(III)-specific exporter proteins as are known for As(i)(III). Our results indicate that the uptake capabilities of arsenic compounds are highly dependent upon the cell type. It may be hypothesized that the arsenic-induced genotoxic effects observed in fibroblasts are due to the high uptake of arsenicals into this cell type. This may explain the high susceptibility of skin fibroblasts to arsenic exposure.
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The title compound, DL-threonine-arsenic acid (1/1), C4H9NO3.H3AsO4, is an unusual adduct containing zwitterionic threonine and neutral arsenic acid molecules. The component species interact by way of N-H...O and O-H...O hydrogen bonds, leading to parallel [001] chains of threonine and arsenic acid molecules which are crosslinked by further O-H...O and N-H...O bonds, resulting in a three-dimensional network.
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Manufacture of an Ayurvedic arsenic-containing compound is described, which is currently in use in India to control blood counts of patients with haematological malignancies. The efficacy and side effects of this compound are evaluated in the light of the fact that arsenic was recognised to be of use in the control of blood counts from patients with chronic myeloid leukaemia as long as 100 years ago, in the West.
It is known that arsenic has different toxicological properties dependent upon both its oxidation state for inorganic compounds, as well as the different toxicity levels exhibited for organic arsenic compounds. The field of arsenic speciation analysis has grown rapidly in recent years, especially with the utilization of high-performance liquid chromatography (HPLC) coupled to inductively coupled plasma mass spectrometry (ICP-MS), a highly sensitive and robust detector system. Complete characterization of arsenic compounds is necessary to understand intake, accumulation, transport, storage, detoxification and activation of this element in the natural environment and living systems. This review describes the essential background and toxicity of arsenic in the environment, and more importantly, some currently used chromatographic applications and sample handling procedures necessary to accurately detect and quantify arsenic in its various chemical forms. Applications and work using only HPLC-ICP-MS for arsenic speciation of environmental and biological samples are presented in this review.
In coal combustion systems, the partitioning of arsenic between the vapor and solid phases is determined by the interaction of arsenic vapors with fly ash compounds under post-combustion conditions. This partitioning is affected by gas-solid reactions between the calcium components of the ash particles and arsenic vapors. In this study, bench scale experiments were conducted with calcium compounds typical of coal-derived fly ash to determine product formation, the extent of reaction and reaction rates when contacted by arsenic oxide vapors. Experiments conducted with arsenic trioxide (As(4)O(6(g))) vapors in contact with calcium oxide, di-calcium silicate and mono-calcium silicate over the temperature range 600-1000 degrees C indicated that these solids were capable of reacting with arsenic vapor species in both air and nitrogen. Calcium arsenate was the observed reaction product in all the samples analyzed. Maximum capture of arsenic occurred at 1000 degrees C with calcium oxide being the most effective of the three solids over the range of temperatures studied. Using a shrinking core model for a first order reaction and the results from intrinsic kinetic experiments conducted in air, the reaction rate constants were found to be 1.4 x 10(-3)exp(-2776/T) m/s for calcium oxide particles, 7.2 x 10(-3)exp(-3367/T) m/s for di-calcium silicate particles and 5.5 x 10(-3)exp(-3607/T) m/s for mono-calcium silicate particles. These results therefore suggest that any calcium present in fly ash can react with arsenic vapor and capture the metal in water-insoluble forms of the less hazardous As(V) oxidation state.
Harmful factors of the industrial environment of the steel plants are represented by sulfur- and arsenic-containing compounds, nitrogen and carbon oxides, aerosols of heavy and rare metals, fluorine compounds whose concentrations exceed the maximum allowable ones in the air of the working place. The results of the cytogenetic examination of metallurgists attest to the pronounced total mutagenic activity of unfavourable factors of the industrial environment, among which the key role is played by arsenic, fluorine and heavy metal compounds.
Human exposure to metals and their compounds may give rise to a number of adverse effects. Of particular interest are such effects that can be elicitated by chronic low-level exposure, since such exposures may occur in human populations both in the general environment and occupationally. The adverse effect that occurs at the lowest exposure has been termed the "critical effect" since it is critical in relation to preventive action aiming at limiting exposures to a safe level. When reviewing the present evidence on the toxicology of metals it becomes evident that "critical effects" may be related to various organ systems, disease categories and biochemical mechanisms of damage. A category of effects, which is of particular interest in relation to critical effects, is hypersensitivity (e.g. with dermal or respiratory manifestations). However conceptual recognition of this category of effects is as yet incomplete. Other important considerations are whether effects display threshold- or non-threshold type dose-response relationships, the latter category obviously being more likely to display a low incidence response at low dose exposure. In this context mutagenic, carcinogenic, developmental and reproductive toxicity of metals are of particular interest. Information on these types of effects compiled during previous meetings of the scientific committee on the toxicilogy of metals and recently updated, indicates that some compounds of arsenic, beryllium, cadmium, chromium and nickel may be regarded as carcinogenic for humans. Available evidence in experimental systems as well as in humans concerning effects of metallic compounds on male and female reproductive systems, congenital teratogenicity and perinatal toxicity as well as effects on the developing central nervous system indicates that such effects should be considered further in relation to critical effects for arsenic, cadmium, lead, mercury and their compounds.
The aim of this study was to determine the dosage and the compounds of arsenic that induce fatty liver in mule ducks and also to investigate their effects on tissue residues. One hundred four ducks, 8 wk old, were randomly selected for one of six dietary treatments in Trial 1 or one of seven dietary treatments in Trial 2. Different levels of roxarsone were administrated: 0, 10, 20, 30, 40, or 50 mg/d, respectively, in Trial 1. In Trial 2, the experimental treatments were of the same level (11.36 mg/d) with different sources of arsenic that included the control without As, roxarsone (3-nitro-4-hydroxyphenylarsonic acid), arsanilic acid, phenylarsonic acid, O-nitro-phenylarsonic acid, As2O3, or As2O5. Both trials lasted 3 wk, with 1 wk on the treatment followed by 2 wk of withdrawal. Results in Trial 1 showed that a dose of 40 mg roxarsone/d increased liver weight and caused fatty liver, whereas administration of 50 mg/d was lethal. In Trial 2, administration of arsenic (11.36 mg/d) for 1 wk significantly depressed feed intake in the roxarsone, As2O3, and As2O5 groups (P < 0.05), whereas the treatment significantly decreased only live weight gain in the roxarsone group (P < 0.05). Administration of roxarsone alone increased (P < 0.05) serum cholesterol (CHOL), albumin (ALB), and total protein (TP), whereas only As2O3 among treatments significantly decreased serum triacylglycerol (TG) concentration (P < 0.05). In the roxarsone, arsanilic acid, and phenylarsonic acid groups, serum high density lipoprotein (HDL) decreased to a greater extent (P < 0.05), and arsanilic acid treatment significantly increased the very low density lipoprotein (VLDL) (P < 0.05). After 2 wk of withdrawal, liver weights and relative liver weights were heavier in the treatment groups of roxarsone, As2O3, and As2O5 as compared to the control (P < 0.05). Levels of CHOL, TG, TP, and ALB were significantly higher in the groups treated with As2O3 or As2O5 as compared to the control (P < 0.05). The roxarsone and arsanilic acid treatments significantly decreased HDL and increased VLDL in plasma (P < 0.05). The creatine kinase (CK) level in the roxarsone, As2O3, and As2O5 groups was significantly higher compared to the control group (P < 0.05). Among the As sources, roxarsone, As2O3, and As2O5 caused fatty liver in mule ducks.
The removal of arsenic(V) from water was investigated under various coagulation conditions and compared to a variety of coagulation agents, including polymeric ferric chloride, polymeric ferric sulfate, polymeric aluminum chloride, polymeric aluminum sulfate, ferric chloride, ferric sulfate, aluminum chloride, and aluminum sulfate. Coagulation conditions evaluated include pH, temperature, type of coagulant, the addition of a coagulation aid, and initial arsenic(V) concentration. Results indicated that the arsenic removal efficiencies of polymeric coagulants were typically 10 to approximately 20% higher than those of their conventional coagulant counterparts.
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The use of arsenic-containing compounds in cancer therapy is currently being re-considered, after the recent approval of arsenic trioxide (Trisenox) for the treatment of relapsed promyelocytic leukemia (PML). In an attempt to prepare a carrier system to minimize the toxicity of this drug, the aim of this study is to prepare and characterize liposomes encapsulating arsenic trioxide (ATO). For this, we prepared different types of liposomes entrapping ATO: large multilamellar (MLV), sonicated (SUV) and dried reconstituted vesicles (DRV). The techniques used were: thin film hydration, sonication and the DRV method, respectively. Two lipid compositions were studied for each liposome type, EggPC/Chol (1:1) and DSPC/Chol (1:1). After liposome preparation, drug encapsulation was evaluated by measuring arsenic in liposomes. For this, energy-dispersive X-ray fluorescence spectroscopy or atomic absorption was used. In addition, the retention of the drug in the liposomes was evaluated after incubating the liposomes in buffer at 37 degrees C. The experimental results reveal that encapsulation of ATO in liposomes ranges between 0.003 and 0.506 mol/ mol of lipid, and is highest in the DRV vesicles and lowest in the small unilamellar vesicles, as anticipated. Considering the in vitro stability of ATO-encapsulating liposomes: 1) For the PC/Chol liposomes (DRV and MLV), after 24 hours of incubation, more than 70% (or 90% in some cases) of the initially encapsulated amount of ATO was released. 2) The liposomes composed of DSPC/Chol could retain substantially higher amounts of ATO, especially the DRV liposomes (54% retained after 24 h). 3) In the case of PC/Chol, temperature of incubation has no effect on the ATO release after 24 hours, but affects the rate of ATO release in the MLV liposomes, while for the DSPC/Chol liposomes there is a slight increase (statistically insignificant) of ATO release at higher temperature.
The gas-phase acidities of methylidynephosphine, HCtbond;P, ethylidynephosphine, CH(3)Ctbond;P, and ethylidynearsine, CH(3)Ctbond;As, have been measured by means of Fourier Transform Ion Cyclotron Resonance (FTICR) mass spectrometry and calculated at the CCSD(T)/6-311+G(3df,2p)//QCISD/ 6-311+G(df,p) level of theory. An analysis of these results shows that, in contrast to the well-known fact that HCtbond;N is a stronger acid than CH(3)Ctbond;N, CH(3)Ctbond;P and CH(3)Ctbond;As are more acidic than HCtbond;P and HCtbond;As, respectively. The most important consequence of this unexpected effect is that while HCtbond;P and HCtbond;As are found to be weaker acids than HCtbond;N, the opposite trend is found for the corresponding methyl derivatives, the acidity of which increases as CH(3)Ctbond;N<CH(3)Ctbond;P<CH(3)Ctbond;As. Also the effects of deprotonation on the structures and the vibrational frequencies of HCtbond;X and CH(3)Ctbond;X (X=N, P, As) compounds are qualitatively similar, but quantitatively very different for nitrogen- as compared with phosphorus- and arsenic-containing compounds. A rationalization of these differences in terms of the bonding differences is presented.
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