Disodium Arsenate Research Articles

Assessment of Phyto-Remediation Quotient of Cultivated Waterleaf Talinum Triangulare on Soil Contaminated With Sodium Arsenate Pesticide

The potential of Waterleaf Talinum triangulare to abstract and consequently remediate As from As-pesticide contaminated soil was investigated by pot experiment and the concentration of As in the plant and soil was determined through mass plasma atomic emission spectroscopy (MP-AES). The composite soil in two separate groups of pots was spiked with 50 mg/kg and 70 mg/kg disodium arsenate pesticide and stands of Waterleaf were grown on them over a 9 weeks growth period. The plant parts (leave and root) and soil after harvesting were pretreated, acid digested and subjected to MP-AES analysis. The results depicted that As concentrations in the plant parts differ at all the treatment levels over the graded period of growth for frequency of harvest and time of harvest and exceeded the maximum permissible limit established by FAO/WHO, and makes the plant unfit for human and animal consumption. The experimental results revealed a statistically significant difference (p<0.05) in the bioaccumulation of As over the graded period of growth at all the treatment levels. The Bio-accumulation factor (BAF) and Bio-concentration factor (BCF) were generally greater than unity (BAF > 1 and BCF > 1) in all treatment levels at the time of harvest which indicates that Waterleaf is suitable for phytoextraction and phytostabilization. However, BAF < 1 and BCF < 1 were observed in the 3rd week and 9th week in the frequency of harvest. Furthermore, Translocation factor (TF <1 and TF > 1) were observed for frequency of harvest and time of harvest, implying that the plant can serve as a bad and good accumulator of As in contaminated soil for phytoremediation if the plant is frequently harvested or allowed to fallow. TF > 1 means that the vegetable will be suitable as a good phytoextractor. It can, therefore, be concluded that Waterleaf can be used for commercial and environmental friendly phytoremediation technology (Green technology) to clean up As polluted sites and environmental monitoring.

Comparison of sensitivity to arsenic compounds between a Bhas 42 cell transformation assay and a BALB/c 3T3 cell transformation assay

A short-term cell transformation assay has recently been developed, using Bhas 42 cells which were established from BALB/c 3T3 cells transfected by v-Ha- ras gene and postulated to be initiated in the two-stage carcinogenesis theory. The Bhas 42 cell transformation assay has been reported to be capable of detecting initiating and promoting activities of chemical carcinogens, according to the different protocols, initiation assay and promotion assay, respectively. The assay is superior to classical transformation assays in cost and labor performance. The present study was carried out to compare its sensitivity with that of a classical BALB/c 3T3 cell system. We performed the Bhas 42 cell transformation assay with inorganic arsenic compounds which are potent environmental carcinogens in human but not mutagens in bacteria or weak mutagens in mammalian cells in vitro. Sodium arsenite, disodium arsenate, and their metabolites, monomethylarsonic acid and dimethylarsinic acid (DMAA) were included in the study. Sodium arsenite was positive in the initiation assay and all compounds except for DMAA were positive in the promotion assay. These results were compared with reported data in a two-stage BALB/c 3T3 cell transformation assay. The sensitivity of Bhas 42 cell transformation assay was found to be similar to that of the conventional BALB/c 3T3 cell transformation assay for the detection of initiating activities of arsenic compounds. For the detection of promoting activities, its sensitivity was equivalent to that of the two-stage BALB/c 3T3 cell transformation assay where the target cells were initiated with sub-threshold dose of 3-methylcholanthrene, confirming that Bhas 42 cells behave as initiated cells in the transformation assay.

A study on carbohydrate moieties of gills and air-breathing organs of the walking catfish Clarias batrachus (Linn.) following exposure to arsenic

The chronic sublethal (1 ppm) effects of an arsenic (As) salt, disodium arsenate heptahydrate (DSA) was examined on the carbohydrate moieties of the gills and air-breathing organs (ABO) of the walking catfish Clarias batrachus Linn. The glycogen content increased quantitatively in the gills during initial stages followed by a decrease after 7 days and throughout treatment. The fall was significant after 30–45 days exposure. This was also accompanied by an increase followed by a decrease in mucogenic activity of the gills. Glycoproteins (GPs) along with the mucous cells stained strongly for carboxylic groups and O-sulfated esters. Unlike the gills, the air-breathing organs showed an increase in glycogen content that surpassed the level of untreated control fish after prolonged exposure. The data indicate that As disturbed aerial respiration after chronic exposure. Mucogenic activity in the air-breathing organs fell markedly and always remained below the level of untreated control fish. Similar to the gills, the air-breathing organs also showed a strong affinity for GPs containing carboxylic groups and O-sulfated esters.

Interaction of arsenic compounds with model phospholipid membranes

This study is part of a project aimed at examining the influence of arsenic on biological membranes. By the use of differential scanning calorimetry (DSC) we have followed the thermotropic behavior of multilamellar vesicles prepared from dimyristoylphosphatidylcholine (DMPC) and dimyristoylphosphatidylethanolamine (DMPE) upon incorporation of sodium arsenite (AsI), disodium arsenate (AsII), cacodylic acid (AsIII) and disodium methyl arsenate (AsIV). The effectiveness of perturbations exerted by various arsenic compounds on thermotropic phase transition was further analysed in terms of thermodynamic parameters: transition temperature, enthalpy and molar heat capacity, determined for lipid/As systems on the basis of heating and cooling scans. It is found that while it only has a slight influence on the thermotropic properties of DMPC, arsenic is able to significantly modify DMPE model membranes.

Inorganic Arsenic Compounds and Methylated Metabolites Induce Morphological Transformation in Two-Stage BALB/c 3T3 Cell Assay and Inhibit Metabolic Cooperation in V79 Cell Assay

We have performed two-stage transformation assay using BALB/c 3T3 cells to determine initiating and promoting activities of disodium arsenate, sodium arsenite, monomethylarsonic acid (MMAA) and dimethylarsinic acid (DMAA). Treatment with these arsenic compounds at the initiating stage induced significant numbers of transformed foci when cells were post-treated with 12-O-tetradecanoylphorbol-13-acetate (TPA). Disodium arsenate was active at the concentrations of 15-30 microM, sodium arsenite 5-20 microM, and DMAA 1-2 mM. MMAA required 10 mM to induce cell transformation. The concentrations of these compounds (except DMAA) that induced transformation were highly growth-inhibitory (more than 50%). DMAA induced transformation foci at growth inhibition levels of 66 to 84%. In experiments on promoting activity, cells pretreated with a sub-threshold dose of 20-methylcholanthrene (MCA, 0.2 microg/ml) or sodium arsenite (10 microM) were used. Transformation was enhanced by post-treatment with disodium arsenate (1-10 microM), sodium arsenite (0.5-2 microM), and MMAA (200-1000 microM), but not with DMAA. Studies of gap junctional intercellular communication using the V79 cell metabolic cooperation assay showed that the arsenic compounds (except DMAA) exhibited inhibitory activity. Thus, most arsenicals were shown to have not only initiating activity, but also promoting activity. In addition, inorganic arsenicals, especially trivalent sodium arsenite, were more active than organic ones and exhibited promoting activity at one-order of magnitude lower than initiating activity. These results suggest that from the viewpoint of human hazard, more attention should be paid to the tumor promoting activity of inorganic arsenic compounds.

Studies on the accumulation and transformation of arsenic in freshwater organisms I. Accumulation, transformation and toxicity of arsenic compounds on the Japanese Medaka, Oryzias latipes

Accumulation, transformation and toxicity of arsenic compounds to Japanese Medaka, Oryzias latipes were investigated. For sodium arsenite [As(III)] and disodium arsenate [As(V)], the mean value for 7-day lethal concentration LC 50 for O. latipes were 14.6 and 30.3 mg As/l, respectively. Direct accumulation of arsenic in O. latipes increased as a function of As(III) concentration in water. A small proportion of accumulated arsenic was transformed to methylated arsenic. As much as 70% of the total arsenic accumulated in tissue was depurated. Accumulation and transformation of As(III) by O. latipes in a simple freshwater food chain were also investigated. The transformation of As(III) to As(V) by organisms was more prevalent than biomethylation of accumulated arsenic in organisms of the three steps of the food chain.

Acute Effect of Orally Administered Gallium Arsenide, Gallium Nitrate and Disodium Arsenate on Heme Synthesis in Male and Female Mice

Gallium arsenide (GaAs), gallium nitrate and disodium arsenate were each administered orally to mice of both sexes (Jcl:ICR strain) at varying dosage levels and examined for their effects on the heme biosynthetic enzyme system in the spleen, liver, kidney and peripheral blood. The results indicate that the areas most affected by administration of gallium nitrate or disodium arsenate were enzymes in the hematogenous cells of mouse spleen. In mice of the disodium arsenate-treated groups δ-aminolevulinic acid synthase (ALAS, EC 2.3.1.37), the first enzyme in the heme biosynthetic pathway and the rate-limiting enzyme for heme synthesis, δ-aminolevulinic acid dehydratase (ALAD, EC 4.2.1.24) and porphobilinogen deaminase (PBGD, EC 4.3.1.8) activities in the spleen were markedly depressed in a dose-dependent fashion. A similar, but apparently less marked, reduction in these enzyme activities in the spleen was also observed in the gallium nitrate-treated groups. The effects of these treatments were more conspicuous in female than in male mice. An in vitro experiment demonstrated that activities of purified ALAS, ALAD and PBGD were not inhibited to any noticeable extent by arsenic compounds. These results suggest that disodium arsenate may strongly inhibit heme biosynthesis in mouse spleen.

Tolerance, bioaccumulation and biotransformation of arsenic in freshwater prawn (Macrobrachium rosenbergii)

Tolerance bioaccumulation and biotransformation of arsenic compounds by a freshwater prawn (Macrobrachium rosenbergii) were investigated. M. rosenbergii was exposed to 10, 20, 30 and 35 μg As cm -3 of disodium arsenate [abbreviated as As(V)], 25, 50, 100 and 120 μg As cm -3 of methylarsonic acid (MMAA), or 100, 200, 300 and 350 μg As cm -3 of dimethylarsinic acid (DMAA). Tolerances (50% lethal concentration : LC 50 ) of the prawn against As(V), MMAA, and DMAA were 30, 100, and 300 μg As cm -3 , respectively. The prawn accumulated arsenic compounds directly from aqueous phase and biotransformed them in part. Both methylation and demethylation of the arsenicals were observed in vivo. Highly methylated and less toxic arsenicals were less accumulated in M. rosenbergii.

Biomethylation and biotransformation of arsenic in a freshwater food chain: Green alga (chlorella vulgaris)→shrimp (neocaridina denticulata)→killifish (oryzias iatipes)

AbstractTolerance, bioaccumulation, biotransformation and excretion of arsenic compounds by the fresh–water shrimp (Neocaridina denticulata) and the killifish (Oryzias latipes) (collected from the natural environment) were investigated. Tolerances (LC50) of the shrimp against disodium arsenate [abbreviated as As(V)], methylarsonic acid (MAA), dimethylarsinic acid (DMAA), and arsenobetaine (AB) were 1.5, 10, 40, and 150μg As ml−1, respectively.N. denticulata accumulated arsenic from an aqueous phase containing 1 μg As ml−1 of As(V), 10 μg As ml−1 of MAA, 30 μg As ml−1 of DMAA or 150 μg As ml−1 of AB, and biotransformed and excreted part of these species. Both methylation and demethylation of the arsenicals were observed in vivo. When living N. denticulata accumulating arsenic was transferred into an arsenic–free medium, a part of the accumulated arsenic was excreted. The concentration of methylated arsenicals relative to total arsenic was higher in the excrement than in the organism.Total arsenic accumulation in each species via food in the food chainGreen algae (Chlorella vulgaris)→ shrimp (N. denticulata)→ killifish (O. latipes)decreased by one order of magnitude or more, and the concentration of methylated arsenic relative to total arsenic accumulated increased successively with elevation in the trophic level. Only trace amounts of monomethylarsenic species were detected in the shrimp and fish tested. Dimethylarsenic species in alga and shrimp, and trimethylarsenic species in killifish, were the predominant methylated arsenic species, respectively.

Different acute effects of oral and intratracheal administration of disodium arsenate and gallium arsenide on heme synthesis in rats

AbstractThe acute influences of arsenic compounds on the metabolism of porphyrins and heme in various organs of rats after oral or intratracheal administration of disodium arsenate (Na2HAsO4) and gallium arsenide (GaAs) were examined and compared.For the oral administration experiments, 21 or 84 mg of Na2HAsO4, or 2 or 4 g of GaAs, per cm3 saline per kg body weight of each animal was administered to Jcl: Wistar male rats and the organs were removed after exsanguination from the vein of the right axilla under anesthesia with ether, 16 h after administration. In the case of intratracheal administration, rats given 8.2 or 16.4 mg of Na2HAsO4, or 0.2 or 0.4 g GaAs per cm3 saline per kg body weight were examined under the same experimental conditions as for the administration route.Increase in the body weight of rats was suppressed after intratracheal administration of the two arsenic compounds. In these rats the hematocrit value increased significantly. These changes were not shown by the orally administered rats. Elevation in δ‐aminolevulinate synthase (ALA‐S, EC 2.3.1.37) activity in erythroblasts by Na2HAsO4 was much higher after intratracheal administration than after oral administration. Suppression in the activities of δ‐aminolevulinate dehydratase (ALA‐D, EC 4.2.1.24) and porphobilinogen deaminase (PBG‐D, EC 4.3.1.8) in peripheral erythrocytes by Na2HAsO4 and GaAs were stronger by intratracheal administration than by the oral route. Influences of GaAs on the activity of PBG‐D in rat liver were shown to be more effective by oral administration than by the intratracheal route. Oral administration of Na2HAsO4 and GaAs had a stronger suppression effect on the activities of ALA‐D and PBG‐D in rat kidney.It seems from these results that the different extents of the influence of arsenic compounds might depend on the routes of intake.

Investigations of the gallbladder pathology associated with dietary exposure to disodium arsenate heptahydrate in juvenile rainbow trout ( Oncorhyncus mykiss)

Juvenile rainbow trout were fed semi-purified diets with (58 μg As/g diet) or without arsenic, added as disodium arsenate heptahydrate (DSA), under standard laboratory conditions for up to 12 weeks, to determine the time-course of development of gallbldder pathology in response to dietary DSA exposure, to correlate this pathology with levels of total arsenic and specific metabolites in the hepatobiliary system and thereby to attempt to gain some insight regarding the mechanism(s) by which the pathological changes develop. Gallbladder lesions associated with this level of dietary arsenic exposure to juvenile rainbow trout include acute inflammation with oedema of the submucosal tissues and sloughing of the epithelium within the first day of exposure, developing to chronic inflammation with fibrosis of the gallbladder wall. These changes may result from the toxic influence of arsenate absorbed into the epithelial cells. The arsenic content of washed gallbladder tissue is a sensitive indicator of recent dietary DSA exposure, while the chronic inflammatory lesion with extensive fibrosis of the gallbladder wall may provide a longer-term indicator of exposure to toxic levels of DSA in the diet of rainbow trout.

Hepatobiliary and hematological effects of dietary disodium arsenate heptahydrate in juvenile rainbow trout ( Oncorhynchus mykiss)

1. The impact of 8–12 weeks exposure to up to 55–60 μg arsenic/g diet as disodium arsenate (DSA) on the hepatobiliary and hematological systems of rainbow trout was assessed. 2. Bile and washed gallbladder tissue arsenic residues in exposed fish were 2–4 times higher than in liver. Plasma arsenic concentration was slightly elevated following dietary DSA exposure. 3. Chronic exposure to dietary DSA caused a mild to moderate responsive anemia. 4. Lipid, but not protein, digestibility after 12 weeks of exposure showed an inverse relationship with severity of gallbladder inflammation in these fish. 5. Changes in the hepatobiliary system appear to provide the most sensitive indicators of dietary DSA exposure in rainbow trout.

Chronic toxicity of dietary disodium arsenate heptahydrate to juvenile rainbow trout (Oncorhynchus mykiss)

Juvenile rainbow trout were fed semi-purified diets containing graded levels of disodium arsenate heptahydrate (DSA) for 12-24 weeks under standard laboratory conditions to define the maximum acceptable toxicant concentration (MATC) and to correlate signs of toxicity with diet and tissue arsenic concentrations. The MATC for DSA was between 13 and 33 micrograms As/g diet or 0.281-0.525 mg As/kg body weight/day. The most sensitive and reliable indicator of chronic dietary DSA toxicity in rainbow trout was chronic inflammation of the gallbladder wall. Chronic inflammatory changes in the sub-epithelial tissues of the gallbladder wall were evident in 71% of rainbow trout exposed to 33 micrograms As/g diet for 24 weeks, and 100% of rainbow trout exposed to 65 micrograms As/g diet for 24 weeks or 49 micrograms As/g diet for 12 weeks. No fish exposed to 13 micrograms As/g diet or less for up to 24 weeks showed any demonstrable gallbladder lesions or any other ill effect of arsenic exposure. Other signs of chronic dietary DSA toxicity to rainbow trout included decreased growth rate, mild to moderate anemia, and, at higher levels of exposure, active feed refusal leading to decreased feed consumption. Mild nephrocalcinosis was noted in one experiment where kidney arsenic residues exceeded 14 micrograms As/g tissue dry weight.

Preliminary investigations on the comparative chronic toxicity of four dietary arsenicals to juvenile rainbow trout ( Salmo gairdneri R.)

Juvenile rainbow trout were fed semi-purified diets in eight-week growth trials to compare the toxicity of four dietary arsenicals: arsenic trioxide (AT); disodium arsenate heptahydrate (DSA); dimethylarsinic acid (DMA); and arsanilic acid (AA). Toxicity responses of reduced growth and feed consumption, and altered feeding behaviour, were noted at all levels of supplementation of AT and DSA (137–1477 μg As/g diet). In contrast, even at the highest levels of supplementation (1497 μg As/g diet as DMA, and 1503 μg As/g diet as AA) the organic arsenicals did not result in these toxicity signs. Carcass arsenic concentration showed a dose-response relationship to dietary arsenic concentration and exposure rate, for each of the arsenicals investigated. At lower levels of exposure, dietary DSA yielded the highest carcass arsenic concentrations, while at higher levels, dietary AT yielded the highest residues. The ‘no observed effect concentration’ (NOEC) for dietary arsenic lies between 1 and 137 μg As/g diet for DSA, between 1 and 180 μg As/g diet for AT, and is at least 1497 μg As/g diet for DMA and AA. It was concluded that disodium arsenate was the most toxic to juvenile rainbow trout of the four dietary arsenicals studied.

The fungicidal properties of certain spray-fluids, IV

The following solutions were tested with respect to their fungicidal properties towards the “powdery,” conidial stage of Sphaerotheca Humuli on young hop-leaves in the greenhouse.(1) A solution of potassium polysulphide containing 0·092 per cent. polysulphide sulphur proved fungicidal, whilst one containing 0·066 per cent. was not quite fungicidal.(2) A solution of sodium polysulphide containing 0·12 per cent. polysulphide sulphur proved fungicidal. It seems probable that solutions of sodium and potassium polysulphides possess the same fungicidal values.(3) Lead arsenate proved to be considerably less fungicidal in action than lead thioarsenate, dicalcium arsenate or disodium arsenate. A solution of lead arsenate containing 0·1 per cent. As2O5 proved to be not quite fungicidal, while one containing 0·204 per cent. As2O5 proved fungicidal.(5) Solutions of calcium polysulphide and of lead arsenate at concentrations below fungicidal strength when mixed together proved to be fungicidal.

The fungicidal properties of certain spray-fluids. III

The following solutions were tested with respect to their fungicidal properties towards the “powdery,” conidial stage of S. Humuli on young hop-leaves in the greenhouse:(1) Disodium arsenate, containing 0·096 per cent. As2O5 proved fungicidal and killed also patches of leaf-cells underlying the mildewpatches, but did not otherwise injure the leaf. A solution containing 0·02 per cent. As2O5 was fungicidal without killing any leaf-cells.(2) Trisodium arsenate containing 0·077 per cent. As2O5 proved fungicidal.(3) Dicalcium arsenate. containing 0·048 per cent. As2O5 proved fungicidal; containing 0·024 per cent. As2O5 the solution was apparently just fungicidal, but with 0·01 per cent. As2O5 the solution was practically non-fungicidal.(4) Tricalcium arsenate containing 0·076 per cent. As2O5 is fungicidal; containing 0·02 per cent. As2O5 it possesses some fungicidal value, but with 0·01 per cent. As2O5 it is practically non-fungicidal.(5) The following constituents of lime-sulphur wash proved nonfungicidal: calcium sulphate, sulphite, thiosulphate, hydroxyhydrosulphide.(6) Calcium polysulphide, at a strength of 0·11 per cent., proved fungicidal.