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PubMed2003

Influence of arsenic co-contamination on DDT breakdown and microbial activity.

The impacts of arsenic co-contamination on the natural breakdown of 1,1,l1-trichloro-2,2-bis(4-chlorophenyl)ethane (DDT) in soil are investigated in a study of 12 former cattle dip sites located in northeastern NSW, Australia. This study examines the relationship between the intrinsic breakdown of DDT to 1,1 -dichloro-2,2-bis(4-chlorophenyl)ethane (DDD) and 1,l-dichloro-2,2-bis(4-chlorophenyl)ethylene (DDE), and the impacts of arsenic co-contamination on this breakdown. Between-site analysis demonstrated that arsenic at 2000 mg/kg gave a 50% reduction in the concentration of DDD compared to background arsenic of 5 mg/kg.Within-site analysis also showed the ratio of DDT:DDD increased in soils as arsenic concentrations increased. This within-site trend was also apparent with the DDT:DDE ratio, suggesting inhibition of DDT breakdown by arsenic co-contamination. Microbial activity was inhibited as residues of total DDTs and arsenic increased. Hence arsenic co-contamination and high concentrations of DDT in soil may result in an increased persistence of DDT in the environment studied.

Animal Husbandry↗
PubMed2002

Mechanisms of arsenic biotransformation.

Inorganic arsenic, a documented human carcinogen, is methylated in the body by alternating reduction of pentavalent arsenic to trivalent and addition of a methyl group from S-adenosylmethionine. Glutathione, and possibly other thiols, serve as reducing agents. The liver is the most important site of arsenic methylation, but most organs show arsenic methylating activity. The end metabolites are methylarsonic acid (MMA) and dimethylarsinic acid (DMA). These are less reactive with tissue constituents than inorganic arsenic and readily excreted in the urine. However, reactive intermediates may be formed. Absorbed arsenate (As(V)) is fairly rapidly reduced in blood to As(III), which implies increased toxicity. Also, intermediate reduced forms of the methylated metabolites, MMA(III) and DMA(III), have been detected in human urine. In particular MMA(III) is highly toxic. To what extent MMA(III) and DMA(III) contribute to the observed toxicity following exposure to inorganic arsenic remains to be elucidated. There are marked differences in the metabolism of arsenic between mammalian species, population groups and individuals. There are indications that subjects with low MMA in urine have faster elimination of ingested arsenic, compared to those with more MMA in urine.

Animals↗
PubMed2001

Changes in properties of adenosine transporters in Trypanosoma evansi and modes of selection of resistance to the melaminophenyl arsenical drug, Mel Cy.

Resistance to arsenical drugs in trypanosomes has been linked to changes in adenosine uptake. The transport of melaminophenyl arsenicals into Trypanosoma brucei was shown to be mediated by an unusual adenosine nucleoside transporter, P2 (Carter and Fairlamb, 1993), and the loss of this transporter is associated with resistance to melaminophenyl arsenicals in these parasites. To further understand the mechanisms of arsenical resistance, we generated several lines of Mel Cy-resistant T. evansi from a drug-sensitive isolate using both in vivo and in vitro selection methods. Uptake of the melaminophenyl arsenical, Mel Cy on the P2 transporter was studied in the drug-sensitive as well as Mel Cy-resistant parasites, by means of inhibition of Mel Cy-induced lysis of trypanosomes, in an in vitro lysis assay. Adenosine uptake was also investigated using competition inhibition assays. Our study shows that T. evansi, TREU 1840, possesses the P1/P2 adenosine transport system as reported in T. brucei and T. equiperdum. However, in T. evansi, the P2 transporter is the larger transport process instead of the P1. The P2 transporter in T. evansi mediated the uptake of Mel Cy in the drug-sensitive parasites. The P2 was retained in all the arsenical-resistant T. evansi lines studied. However, the activity of the transporter was reduced to different extents in the different-resistant lines. The residual P2 activity related well to the levels of drug resistance in each line, suggesting that P2 activity could be an important marker for arsenical resistance. Furthermore, important differences were observed between the in vivo- and the in vitro-selected arsenical-resistant parasites suggesting that there may be differences in resistance phenotypes selected on the field.

Adenine↗
PubMed2002

Differential effects of arsenic on folate binding protein 2 (Folbp2) null and wild type fibroblasts.

Exposure to arsenic results in a wide variety of adverse effects. It has been postulated that one mechanism of arsenic toxicity is disruption of cellular methyl biochemistry. Because dietary folate is required to generate the methyl donor S-adenosyl methionine, we hypothesized that loss of folate binding protein 2 (Folbp2) results in increased susceptibility to arsenic-induced cytotoxicity. Using Folbp2 +/+ and -/- fibroblasts, we determined that Folbp2 null cells display increased sensitivity to arsenic exposure. Folic acid supplementation partially rescues wild type cells from arsenic toxicity, but Folbp2 null cells are not protected. Arsenic inhibits folic acid uptake in Folbp2 null fibroblasts, but not wild type cells; baseline uptake is similar in both cell types. These results support the possibility that arsenic toxicity occurs, in part, by perturbing cellular methyl biochemistry. Furthermore, identification of Folbp2 as a protective protein presents an opportunity to identify populations at increased risk for serious effects of arsenic exposure.

Animals↗
PubMed2003

Oxidative stress as a possible mode of action for arsenic carcinogenesis.

Many modes of action for arsenic carcinogenesis have been proposed, but few theories have a substantial mass of supporting data. Three stronger theories of arsenic carcinogenesis are production of chromosomal abnormalities, promotion of carcinogenesis and oxidative stress. This article presents the oxidative stress theory along with some supporting experimental data. In the area of which arsenic species is causually active, recent data have suggested that trivalent methylated arsenic metabolites, particularly monomethylarsonous acid (MMA(III)) and dimethylarsinous acid (DMA(III)), have a great deal of biological activity. Some evidence now indicates that these trivalent, methylated, and relatively less ionizable arsenic metabolites may be unusually capable of interacting with cellular targets such as proteins and even DNA. Thus for inorganic arsenic, oxidative methylation followed by reduction to trivalency may be a activation, rather than a detoxification pathway. This would be particularly true for arsenate. In forming toxic and carcinogenic arsenic species, reduction from the pentavalent state to the trivalent state may be as or more important than methylation of arsenic.

Animals↗
PubMed1999

Arsenic binding proteins from human lymphoblastoid cells.

Arsenic is a ubiquitous contaminant of drinking water and food. The mechanisms of the toxic action of inorganic arsenic are unknown. We report the isolation of proteins having a high affinity for arsenic in the +3 oxidation state that are induced by arsenite (AsIII) in human lymphoblastoid cells. The arsenic-binding proteins were isolated using a p-aminophenylarsine oxide affinity column. At least four proteins of 50, 42, 38.5 and 19.5 kDa were isolated by elution with 10 or 100 mM 2-mercaptoethanol. Two proteins were tentatively identified as tubulin and actin on the basis of their molecular weights and previously reported affinity for the arsenic column. The identities of the remaining proteins are unknown. Heme oxygenase 1 was induced by AsIII but did not bind to the arsenic affinity column. We conclude that AsIII induces multiple proteins that have variable affinities for arsenic in the +3 state as judged by the concentration of 2-mercaptoethanol required for their elution. The arsenic binding motif of these proteins may involve three thiol groups arranged 3-6 A apart by the tertiary structure of the protein as suggested by others. These proteins may serve as high affinity binding sites for AsIII and may be involved in the biological action of AsIII.

Actins↗
PubMedDate not supplied

Human sperm immobilizing activity of aminophenyl arsenic acid and its N-substituted quinazoline, pyrimidine, and purine derivatives: protective effect of glutathione.

We examined the potential toxicity of pentavalent organic arsenicals for human sperm. We used computer-assisted sperm analysis to examine the effects of three aminophenyl arsenicals and their nine N-substituted quinazoline, pyrimidine, and purine derivatives on human sperm motility and kinematics in human semen and medium. Among the arsenicals examined, (aminophenylazo)-phenyl arsonic acid and its N-substituted pyrimidine derivative PHI-370 (2-methylthio-4-[(4'-aminophenylazo)-phenylarsonic acid] pyrimidine) exhibited rapid sperm immobilizing activity in medium with EC(50) values of 77 and 82 microM, respectively, and t(1/2) of < 3 min. Molecular modeling analysis indicated that sperm-immobilizing organic arsenicals exhibit high dipole moments (>7 Debyes). Sperm immobilizing activity of these arsenicals was completely abrogated in the presence of seminal plasma. Furthermore, coincubation of motile sperm with PHI-370 in the presence of reduced glutathione (GSH) resulted in dose-dependent protection of sperm motility and sperm motion parameters. Coincubation of the arsenical with GSH at a molar ratio of 1:20 resulted in 95% retention of sperm progressive motility. The mean values of the other sperm movement characteristics also showed > 90% protection. These observations suggest that the rapid sperm immobilizing activity of these pentavalent arsenicals may be as a result of direct binding of the arsenical with the sperm thiol components essential for sperm motility as well as induction of oxidative damage by disruption of sperm cell's antioxidant system. Sodium arsanilate and its N-substituted pyrimidine derivative, PHI-370, are useful probes to further evaluate the mechanism of pentavalent arsanilate-induced human sperm dysfunction.

Arsanilic Acid↗
PubMed1999

Arsenic speciation in human urine reference materials using high-performance liquid chromatography with inductively coupled plasma mass spectrometric detection.

Six arsenic compounds including arsenocholine, arsenobetaine, dimethylarsinic acid, methylarsonic acid, arsenous acid and arsenic acid were separated by high-performance liquid chromatography (HPLC) on a Hamilton PRP-X100 anion-exchange column using isocratic elution and detected by inductively coupled plasma mass spectrometry (ICP-MS). This analytical procedure was applied to the speciation of arsenic compounds in human urine. The influence of urine matrix on the separation of arsenic compounds was evaluated and the determination of arsenic compounds was not hampered by the ArCl interference which has often been encountered in ICP-MS. Three human urine reference materials, SRM 2670 normal level, SRM 2670 elevated level and Lyphocheck urine metal control 1, were analyzed with respect to arsenic compounds by HPLC-ICP-MS. The results were found to be in good agreement with the certified total arsenic concentration in the reference materials. Six arsenic compounds were detected. Arsenobetaine was found to be present in all of the investigated human urine reference materials.

Arsenic↗
PubMed2002

Enhanced frequency of micronuclei in individuals exposed to arsenic through drinking water in West Bengal, India.

In West Bengal, India arsenic in ground water has been found to be above the maximum permissible limit in seven districts covering an area of 37,493km2. In the present study, evaluation of the micronuclei (MN) formation in oral mucosa cells, urothelial cells and peripheral blood lymphocytes was carried out in the symptomatic individuals exposed to arsenic through drinking water. Forty five individuals with cutaneous signs of arsenicism from four affected districts (368.11 microg/l of As in drinking water) were considered as the exposed group and 21 healthy individuals with no symptoms of arsenic poisoning and residing in two unaffected districts (5.49 microg/l of As) were considered as controls. The exposed and control groups had similar age distribution and socioeconomic status. Standardised questionnaires were utilised and medical examination was conducted to ascertain exposure history, sociodemographic characteristics, diet, health, medication, addiction and chief symptoms in the study participants. Arsenic exposure was confirmed by measuring the arsenic content in the drinking water, nails, hair and urine samples from the volunteers. Arsenic contents in the urine, nail and hair in the exposed group were 24.45 microg/l, 12.58 and 6.97 microg/g, respectively which were significantly high in comparison to corresponding control group values of 4.88 microg/l, 0.51 and 0.34 microg/g, respectively. Exposed individuals showed a statistically significant increase in the frequency of MN in oral mucosa, urothelial cells and lymphocytes (5.15, 5.74 and 6.39/1000 cells, respectively) when compared with the controls (0.77, 0.56 and 0.53/1000 cells, respectively). Thus, the above results indicate that the symptomatic individuals exposed to arsenic through drinking water in this region have significant cytogenetic damage.

Adolescent↗
PubMed1997

Arsenic can mediate skin neoplasia by chronic stimulation of keratinocyte-derived growth factors.

Although numerous epidemiological studies have shown that inorganic arsenicals are human skin carcinogens, there is currently no accepted mechanism for its action or an established animal model for its study. We observed increased mRNA transcripts and secretion of keratinocyte growth factors, including granulocyte macrophage-colony stimulating factor (GM-CSF) and transforming growth factor-alpha (TGF-alpha) and the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in primary human epidermal keratinocytes cultured in the presence of low micromolar concentrations of sodium arsenite. Total cell numbers, as well as c-myc expression and incorporation of [3H]thymidine, both indicators of cell proliferation, were also elevated in keratinocyte cultures treated with sodium arsenite. As an in vivo model, the influence of arsenic on mouse skin tumor development was studied in transgenic TG.AC mice which carry the v-Ha-ras oncogene, and can serve as a genetically initiated model for skin carcinogenesis. Following low-dose application of 12-O-tetradecanoyl phorbol-13-acetate (TPA), a marked increase in the number of skin papillomas occurred in transgenic mice receiving arsenic in the drinking water as compared to control drinking water. Papillomas did not develop in arsenic-treated transgenic mice that had not received TPA or arsenic-treated wild-type FVB/N mice, suggesting that arsenic is neither a tumor initiator or promoter but rather an enhancer. Injection of anti-GM-CSF antibodies following application of TPA in transgenic mice reduced the number of papillomas. Consistent with that observed in human keratinocyte cultures, increases in GM-CSF and TGF-alpha mRNA transcripts were found within the epidermis of arsenic-treated mice when compared to controls within 6 weeks of treatment. These results suggest that arsenic enhances papilloma development via the chronic stimulation of keratinocyte-derived growth factors and represents the first example of a chemical carcinogen that acts in this manner. These studies suggest that in vitro studies with human keratinocyte cultures examined in conjunction with TG.AC transgenic mice can provide a useful model for examining the tumor enhancing properties of environmental chemicals.

Animals↗
PubMed2003

Oxidative stress by inorganic arsenic: modulation by thyroid hormones in rat.

Arsenic toxicity is attributed mainly to lipid peroxidation and oxidative stress. We therefore studied the modulatory effects of thyroid hormones on arsenic toxicity in rat on lipid peroxidation and oxidative stress. Thyroid hormones, through a mechanism unknown at present, inhibit arsenic accumulation in liver and kidney. Mobilization of arsenic apparently diminishes lipid peroxidation and improves reduced glutathione status, two biochemical demands of combating arsenic toxicity. Results are discussed in reference to the effect of thyroid hormones on microsomal metabolism of arsenic. Arsenic is less toxic in hyperthyroid than in hypothyroid rats. A physiological antagonism between arsenic and thyroxine is discussed.

Analysis of Variance↗
PubMed2001

Capture of gas-phase arsenic oxide by lime: kinetic and mechanistic studies.

Trace metal emission from coal combustion is a major concern for coal-burning utilities. Toxic compounds such as arsenic species are difficult to control because of their high volatility. Mineral sorbents such as lime and hydrated lime have been shown to be effective in capturing arsenic from the gas phase over a wide temperature range. In this study, the mechanism of interaction between arsenic oxide (As2O3) and lime (CaO) is studied over the range of 300-1000 degrees C. The interaction between these two components is found to depend on the temperature; tricalcium orthoarsenate (Ca3As2O8) is found to be the product of the reaction below 600 degrees C, whereas dicalcium pyroarsenate (Ca2As2O7) is found to be the reaction product in the range of 700-900 degrees C. Maximum capture of arsenic oxide is found to occur in the range of 500-600 degrees C. At 500 degrees C, a high reactivity calcium carbonate is found to capture arsenic oxide by a combination of physical and chemical adsorption. Intrinsic kinetics of the reaction between calcium oxide and arsenic oxide in the medium-temperature range of 300-500 degrees C is studied in a differential bed flow-through reactor. Using the shrinking core model, the order of reaction with respect to arsenic oxide concentration is found to be about 1, and the activation energy is calculated to be 5.1 kcal/mol. The effect of initial surface area of CaO sorbent is studied over a range of 2.7-45 m2/g using the grain model. The effect of other major acidic flue gas species (SO2 and HCl) on arsenic capture is found to be minimal under the conditions of the experiment.

Adsorption↗
PubMed2004

Accumulation of arsenic in drinking water distribution systems.

The tendency for iron solid surfaces to adsorb arsenic is well-known and has become the basis for several drinking water treatment approaches that remove arsenic. It is reasonable to assume that iron-based solids, such as corrosion deposits present in drinking water distribution systems, have similar adsorptive properties and could therefore concentrate arsenic and potentially re-release it into the distribution system. The arsenic composition of solids collected from drinking water distribution systems (pipe sections and hydrant flush solids), where the waters had measurable amounts of arsenic in their treated water, were determined. The elemental composition and mineralogy of 67 solid samples collected from 15 drinking water utilities located in Ohio (7), Michigan (7), and Indiana (1) were also determined. The arsenic content of these solids ranged from 10 to 13 650 microg of As/g of solid (as high as 1.37 wt %), and the major element of most solids was iron. Significant amounts of arsenic were even found in solids from systems that were exposed to relatively low concentrations of arsenic (<10 microg/L) in the water.

Adsorption↗
PubMed2006

Arsenic sequestration in iron plaque, its accumulation and speciation in mature rice plants (Oryza sativa L.).

A compartmented soil-glass bead culture system was used to investigate characteristics of iron plaque and arsenic accumulation and speciation in mature rice plants with different capacities of forming iron plaque on their roots. X-ray absorption near-edge structure spectra and extended X-ray absorption fine structure were utilized to identify the mineralogical characteristics of iron plaque and arsenic sequestration in plaque on the rice roots. Iron plaque was dominated by (oxyhydr)oxides, which were composed of ferrihydrite (81-100%), with a minor amount of goethite (19%) fitted in one of the samples. Sequential extraction and XANES data showed that arsenic in iron plaque was sequestered mainly with amorphous and crystalline iron (oxyhydr)oxides, and that arsenate was the predominant species. There was significant variation in iron plaque formation between genotypes, and the distribution of arsenic in different components of mature rice plants followed the following order: iron plaque > root > straw > husk > grain for all genotypes. Arsenic accumulation in grain differed significantly among genotypes. Inorganic arsenic and dimethylarsinic acid (DMA) were the main arsenic species in rice grain for six genotypes, and there were large genotypic differences in levels of DMA and inorganic arsenic in grain.

Absorptiometry, Photon↗
PubMed2002

Vegetables collected in the cultivated Andean area of northern Chile: total and inorganic arsenic contents in raw vegetables.

High levels of arsenic are found in the soil and water of the Second Region in Chile as a result of natural causes. Total and inorganic arsenic contents were analyzed in the edible part of 16 agricultural products (roots, stems, leaves, inflorescences, and fruits) grown in this area. The total arsenic contents varied in the range 0.008-0.604 microg g(-1) of wet weight (ww), below the maximum level allowed by Chilean legislation (1 microg(-1) of ww). Inorganic arsenic contents (range = 0.008-0.613 microg(-1) of ww) represented between 28 and 114% of total arsenic. The concentrations of total and inorganic arsenic found in edible roots and leaves were higher than those found in fruit. The highest concentrations were found in a sample of spinach. High quantities of this vegetable would have to be consumed (250 g/day) to reach the Provisional Tolerable Weekly Intake for inorganic arsenic. The vegetable group may make a considerable contribution to the total intake of inorganic arsenic.

Arsenic↗
PubMed2001

In vitro effect of arsenical compounds on glutathione-related enzymes.

The mechanism of arsenic toxicity is believed to be due to the ability of arsenite (As(III)) to bind protein thiols. Glutathione (GSH) is the most abundant cellular thiol, and both GSH and GSH-related enzymes are important antioxidants that play an important role in the detoxification of arsenic and other carcinogens. The effect of arsenic on the activity of a variety of enzymes that use GSH has been determined using purified preparations of glutathione reductase (GR) from yeast and bovine glutathione peroxidase (GPx) and equine glutathione S-transferase (GST). The effect on enzyme activity of increasing concentrations (from 1 microM to 100 mM) of commercial sodium arsenite (As(III)) and sodium arsenate (As(V)) and a prepared arsenic(III)-glutathione complex [As(III)(GS)(3)] and methylarsenous diiodide (CH(3)As(III)) has been examined. GR, GPx, and GST are not sensitive to As(V) (IC(50) > 50 mM), and none of the enzymes are inhibited or activated by physiologically relevant concentrations of As(III), As(III)(GS)(3), or CH(3)As(III), although CH(3)As(III) is the most potent inhibitor (0.3 mM < IC(50) < 1.5 mM). GPx is the most sensitive to arsenic treatment and GST the least. Our results do not implicate a direct interaction of As with the glutathione-related enzymes, GR, GPx, and GST, in the mechanism of arsenic toxicity. CH(3)As(III) is the most effective inhibitor, but it is unclear whether this product of arsenic metabolism is produced at a sufficiently high concentration in critical target tissues to play a major role in either arsenic toxicity or carcinogenesis.

Arsenicals↗
PubMed2004

Role of metal-reducing bacteria in arsenic release from Bengal delta sediments.

The contamination of ground waters, abstracted for drinking and irrigation, by sediment-derived arsenic threatens the health of tens of millions of people worldwide, most notably in Bangladesh and West Bengal. Despite the calamitous effects on human health arising from the extensive use of arsenic-enriched ground waters in these regions, the mechanisms of arsenic release from sediments remain poorly characterized and are topics of intense international debate. We use a microscosm-based approach to investigate these mechanisms: techniques of microbiology and molecular ecology are used in combination with aqueous and solid phase speciation analysis of arsenic. Here we show that anaerobic metal-reducing bacteria can play a key role in the mobilization of arsenic in sediments collected from a contaminated aquifer in West Bengal. We also show that, for the sediments in this study, arsenic release took place after Fe(III) reduction, rather than occurring simultaneously. Identification of the critical factors controlling the biogeochemical cycling of arsenic is one important contribution to fully informing the development of effective strategies to manage these and other similar arsenic-rich ground waters worldwide.

Aerobiosis↗
PubMed2003

Environmental monitoring of historical change in arsenic deposition with tree bark pockets.

ICP-MS analysis recorded historical change (c. 1846 to 2002) in the arsenic concentration of bark included within the trunks (tree bark pockets) of two Japanese oak trees (Quercus crispula), collected at an elevated location approximately 10 km from the Ashio copper mine and smelter, Japan. The arsenic concentration of the bark pockets was 0.016 +/- 0.003 microg cm(-2) c. 1846 (n = 5) and rose 50-fold from c. 1875 to c. 1925, from approximately 0.01 to 0.5 microg cm(-2). The rise coincided with increased copper production in Ashio from local sulfide ores, from 46 tons per year in 1877 to 16,500 tons per year in 1929. Following a decline in arsenic concentration and copper production, in particular during the Second World War, a second peak was observed c. 1970, corresponding to high levels of production from both local (6,000 tons per year) and imported (30,000 tons per year) ores, smelted from 1954. Compared to the local ores, the contribution of arsenic from imported ores appeared relatively low. Arsenic concentrations declined from c. 1970 to the present following the closure of the mine in 1974 and smelter in 1989, recording 0.058 +/- 0.040 microg cm(-2) arsenic (n = 5) in surface bark collected in 2002. The coincident trends in arsenic concentration and copper production indicated that the bark pockets provided an effective record of historical change in atmospheric arsenic deposition.

Air Pollutants↗