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PubMed2005

Antioxidant responses of hyper-accumulator and sensitive fern species to arsenic.

Plant species capable of hyper-accumulating heavy metals are of considerable interest for phytoremediation, and differ in their ability to accumulate metals from the environment. This work aims to examine (i) arsenic accumulation in three fern species [Chinese brake fern (Pteris vittata L.), slender brake fern (Pteris ensiformis Burm. f.), and Boston fern (Nephrolepis exaltata L.)], which were exposed to 0, 150, or 300 muM of arsenic (Na(2)HAsO(4).7H(2)O), and (ii) the role of anti-oxidative metabolism in arsenic tolerance in these fern species. Arsenic accumulation increased with an increase in arsenic concentration in the growth medium, the most being found in P. vittata fronds showing no toxicity symptoms. In addition, accumulation was highest in the fronds, followed by the rhizome, and finally the roots, in all three fern species. Thiobarbituric acid-reacting substances, indicators of stress in plants, were found to be lowest in P. vittata, which corresponds with its observed tolerance to arsenic. All three ferns responded differentially to arsenic exposure in terms of anti-oxidative defence. Higher levels of superoxide dismutase, catalase, and ascorbate peroxidase were observed in P. vittata than in P. ensiformis and N. exaltata, showing their active involvement in the arsenic detoxification mechanism. However, no significant increase was observed in either guaiacol peroxides or glutathione reductase in arsenic-treated P. vittata. Higher activity of anti-oxidative enzymes and lower thiobarbituric acid-reacting substances in arsenic-treated P. vittata correspond with its arsenic hyper-accumulation and no symptoms of toxicity.

Antioxidants↗
PubMed2006

Relative oral bioavailability of arsenic from contaminated soils measured in the cynomolgus monkey.

A number of studies have found that gastrointestinal absorption of arsenic from soil is limited, indicating that a relative oral bioavailability (RBA) adjustment is warranted when calculating risks from exposure to arsenic-contaminated soil. However, few studies of arsenic bioavailability from soil have been conducted in animal models with phylogenetic similarity to humans, such as nonhuman primates. We report here the results of a study in which the RBA of arsenic in soil from a variety of types of contaminated sites was measured in male cynomolgus monkeys. A single oral dose of each contaminated soil was administered to five adult male cynomolgus monkeys by gavage, and the extent of oral absorption was evaluated through measurement of arsenic recovery in urine and feces. Urinary recovery of arsenic following doses of contaminated soil was compared with urinary recovery following oral administration of sodium arsenate in water in order to determine the RBA of each soil. RBA of arsenic in 14 soil samples from 12 different sites ranged from 0.05 to 0.31 (5-31%), with most RBA values in the 0.1-0.2 (10-20%) range. The RBA values were found to be inversely related to the amount of arsenic present with iron sulfate. No other significant correlations were observed between RBA and arsenic mineralogic phases in the test soils. The lack of clear relationships between arsenic mineralogy and RBA measured in vivo suggests that gastrointestinal absorption of arsenic from soil may be more complex than originally thought, and subject to factors other than simple dissolution behavior.

Animals↗
PubMed2000

Associations between drinking water and urinary arsenic levels and skin lesions in Bangladesh.

The present study examined the associations between drinking water and urinary arsenic levels and skin lesions among 167 residents of three contiguous villages in Bangladesh. Thirty-six (21.6%) had skin lesions (melanosis, hyperkeratosis, or both), of which 13 (36.1%) occurred in subjects who were currently drinking water containing concentrations of arsenic < 50 micrograms/L. The risk for skin lesions in relation to the exposure estimates based on urinary arsenic was elevated more than 3-fold, with the odds ratios for the highest versus the lowest quartiles being 3.6 (95% confidence interval, 1.2 to 12.1) for urinary total arsenic and 3.2 (95% confidence interval, 1.1 to 10.0) for urinary creatinine-adjusted total arsenic. The risks for skin lesions in relation to the exposure estimates based on arsenic in drinking water were less strongly elevated, with the odds ratios for the highest versus the lowest quartiles of exposure being 1.7 (95% confidence interval, 0.6 to 5.1) for drinking-water arsenic and 2.3 for cumulative arsenic index. The study suggests that arsenic exposure is associated with skin lesions in the Bangladesh population and that urinary arsenic may be a stronger predictor of skin lesions than arsenic in drinking water in this population.

Adult↗
PubMed2006

Modification of risk of arsenic-induced skin lesions by sunlight exposure, smoking, and occupational exposures in Bangladesh.

BACKGROUND: The risk of skin lesions associated with arsenic exposure from drinking water in Bangladesh is considerably greater in men than in women. METHODS: Using baseline data from 11,062 cohort members in the Health Effects of Arsenic Longitudinal Study in Araihazar, Bangladesh, we performed a cross-sectional analysis to evaluate whether the association between arsenic exposure from drinking water and the risk of skin lesions is modified by tobacco smoking, excessive sunlight, the use of fertilizer, and the use of pesticides. A time-weighted well arsenic concentration was estimated for each participant by incorporating history of well use. Relative excess risk for interaction (RERI) and its 95% confidence intervals (CIs) were estimated using adjusted prevalence odds ratios. RESULTS: We observed a synergistic effect between the highest level of arsenic exposure (> 113 microg/L) and tobacco smoking on risk of skin lesions in men (RERI = 1.5 [95% CI = 0.3 to 2.7] overall and 1.7 [0.2 to 3.4] for the subpopulation with longer-term arsenic exposure). We also observed suggestive synergistic effects between higher levels (28.1-113.0 microg/L and 113.1-864.0 microg/L) of arsenic exposure and fertilizer use in men (RERI = 1.0 [-0.2 to 2.2] and 1.3 [-0.2 to 2.9] respectively). Furthermore, the risk of skin lesions associated with any given level of arsenic exposure was greater in men with excessive sun exposure. The patterns of effect estimates in women indicate similar-but-weaker interaction effects of arsenic exposure with tobacco smoking and fertilizer use. CONCLUSIONS: These findings help explain why the risk of arsenic-related skin lesions was much greater in men than in women in Bangladesh. Because most arsenic-induced skin cancers arise from these skin lesions, treatment and remediation plans should take into consideration these etiologic cofactors.

Adult↗
PubMed2004

Children's exposure to arsenic from CCA-treated wooden decks and playground structures.

CCA-treated wood is widely used in the fabrication of outdoor decks and playground equipment. Because arsenic can be removed from the surface of CCA-treated wood both by physical contact and by leaching, it is important to determine whether children who play on such structures may ingest arsenic in quantities sufficient to be of public health concern. Based on a review of existing studies, it is estimated that arsenic doses in amounts of tens of micrograms per day may be incurred by children having realistic levels of exposure to CCA-treated decks and playground structures. The most important exposure pathway appears to be oral ingestion of arsenic that is first dislodged from the wood by direct hand contact, then transferred to the mouth by children's hand-to-mouth activity. The next most important pathway appears to be dermal absorption of arsenic, while ingestion of soil that has become contaminated by leaching from CCA-treated structures appears to be of lesser importance, except possibly in the case of children with pica. Considerable uncertainty, however, is associated with quantitative estimates of children's arsenic exposure from CCA-treated wood. Priorities for refining estimates of arsenic dose include detailed studies of the hand-to-mouth transfer of arsenic, studies of the dermal and gastrointestinal absorption of dislodgeable arsenic, and studies in which doses of arsenic to children playing in contact with CCA-treated wood are directly determined by measurement of arsenic in their urine, hair, and nails.

Arsenates↗
PubMed1996

Geographical and temporal differences in the urinary excretion of inorganic arsenic: a Belgian population study.

OBJECTIVE: This Belgian study assessed the geographical and temporal differences in the exposure of the population to inorganic arsenic, a known carcinogen. METHODS: In the CadmiBel study (1985-9) the 24 h urinary arsenic excretion was measured, as an index of recent exposure, in industrialised cities (Liège: n = 664, Charleroi: n = 291), in a rural control area (Hechtel-Eksel: n = 397), and in rural districts in which the population had possibly been exposed through the drinking water or the emissions of nonferrous smelters (Wezel: n = 93, Lommel: n = 111, and Pelt: n = 133). In the PheeCad study, in 1991-5, the rural areas (n = 609) were re-examined together with an urban control area (Leuven: n = 152). RESULTS: The CadmiBel results showed that after adjustment for sex, age, and body mass index, the 24 h arsenic excretion was on average low in Liège (91 nmol), Charleroi (155 nmol), Hechtel-Eksel (144 nmol), and Wezel (158 nmol), whereas the highest excretions were found in Lommel (570 nmol) and Pelt (373 nmol). During the PheeCad study, the mean 24 h arsenic excretion in the rural areas ranged from 81 to 111 nmol. This was lower than six years earlier and similar to the excretion in the control town (108 nmol). Longitudinal studies in 529 people living in the rural areas confirmed that their 24 h arsenic excretion had decreased (P < 0.001) from 222 to 100 nmol. As well as the drinking water, industry was likely to be a source of the increased exposure in Lommel and Pelt in 1985-9, because at that time the urinary arsenic excretion did not follow the regional differences in the arsenic content of the drinking water, because the fall in the arsenic excretion over time coincided with the implementation by industry of stricter environmental regulations, because in individual subjects the urinary arsenic excretion was inversely correlated with the distance to the nearest smelter, and because an increased arsenic excretion was only found downwind from the main smelter. The official network that monitors the arsenic concentration in airborne and fall out dust did not detect the high exposure in Lommel and Pelt between 1985 and 1989. CONCLUSION: This study highlights the necessity to validate environmental monitoring programmes by directly estimating the internal exposure of the population.

Adult↗
PubMed2006

Gene expression profiles in peripheral lymphocytes by arsenic exposure and skin lesion status in a Bangladeshi population.

Millions of individuals worldwide are chronically exposed to arsenic through their drinking water. In this study, the effect of arsenic exposure and arsenical skin lesion status on genome-wide gene expression patterns was evaluated using RNA from peripheral blood lymphocytes of individuals selected from the Health Effects of Arsenic Longitudinal Study. Affymetrix HG-U133A GeneChip (Affymetrix, Santa Clara, CA) arrays were used to measure the expression of approximately 22,000 transcripts. Our primary statistical analysis involved identifying differentially expressed genes between participants with and without arsenical skin lesions based on the significance analysis of microarrays statistic with an a priori defined 1% false discovery rate to minimize false positives. To better characterize differential expression, we also conducted Gene Ontology and pathway comparisons in addition to the gene-specific analyses. Four-hundred sixty-eight genes were differentially expressed between these two groups, from which 312 differentially expressed genes were identified by restricting the analysis to female never-smokers. We also explored possible differential gene expression by arsenic exposure levels among individuals without manifest arsenical skin lesions; however, no differentially expressed genes could be identified from this comparison. Our findings show that microarray-based gene expression analysis is a powerful method to characterize the molecular profile of arsenic exposure and arsenic-induced diseases. Genes identified from this analysis may provide insights into the underlying processes of arsenic-induced disease and represent potential targets for chemoprevention studies to reduce arsenic-induced skin cancer in this population.

Adult↗
PubMed2000

Groundwater arsenic contamination in Bangladesh and West Bengal, India.

Nine districts in West Bengal, India, and 42 districts in Bangladesh have arsenic levels in groundwater above the World Health Organization maximum permissible limit of 50 microg/L. The area and population of the 42 districts in Bangladesh and the 9 districts in West Bengal are 92,106 km(2) and 79.9 million and 38,865 km(2) and 42.7 million, respectively. In our preliminary study, we have identified 985 arsenic-affected villages in 69 police stations/blocks of nine arsenic-affected districts in West Bengal. In Bangladesh, we have identified 492 affected villages in 141 police stations/blocks of 42 affected districts. To date, we have collected 10,991 water samples from 42 arsenic-affected districts in Bangladesh for analysis, 58,166 water samples from nine arsenic-affected districts in West Bengal. Of the water samples that we analyzed, 59 and 34%, respectively, contained arsenic levels above 50 microg/L. Thousands of hair, nail, and urine samples from people living in arsenic-affected villages have been analyzed to date; Bangladesh and West Bengal, 93 and 77% samples, on an average, contained arsenic above the normal/toxic level. We surveyed 27 of 42 districts in Bangladesh for arsenic patients; we identified patients with arsenical skin lesions in 25 districts. In West Bengal, we identified patients with lesions in seven of nine districts. We examined people from the affected villages at random for arsenical dermatologic features (11,180 and 29,035 from Bangladesh and West Bengal, respectively); 24.47 and 15.02% of those examined, respectively, had skin lesions. After 10 years of study in West Bengal and 5 in Bangladesh, we feel that we have seen only the tip of iceberg.

Arsenic↗
PubMed2002

Pathology related to chronic arsenic exposure.

Millions now suffer the effects of chronic arseniasis related to environmental arsenic exposure. The biological mechanisms responsible for arsenic-induced toxicity and especially chronic effects, including cancer, are not well known. The U.S. Armed Forces Institute of Pathology (AFIP) is participating in an international research effort to improve this understanding by the development of the International Tissue and Tumor Repository for Chronic Arsenosis (ITTRCA). The ITTRCA obtains, archives, and makes available for research purposes, tissues from subjects exposed to arsenic. We provide here a short overview of arsenic-induced pathology, briefly describe arsenic-induced lesions in the skin and liver, and present five case reports from the ITTRCA. Arsenic-induced skin pathology includes hyperkeratosis, pigmentation changes, Bowen disease, squamous cell carcinoma, and basal cell carcinomas. A unique spectrum of skin lesions, known as arsenical keratosis, is rather characteristic of chronic arseniasis. Bowen disease, or squamous cell carcinoma in situ of the skin, has been well documented as a consequence of arsenical exposure. A spectrum of liver lesions has also been attributed to chronic arseniasis. Of these, hepatocellular carcinoma, angiosarcoma, cirrhosis, and hepatoportal sclerosis have been associated with arsenic exposure. We present case reports that relate to these health conditions, namely, squamous cell carcinoma, basal cell carcinoma, and Bowen disease of the skin and hepatocellular carcinoma and angiosarcoma of the liver. Four patients had been treated with arsenical medications for such conditions as asthma, psoriasis, and syphilis, and one case occurred in a boy chronically exposed to arsenic in drinking water.

Adolescent↗
PubMed1977

Experimental studies on arsenic absorption routes in rats.

Pentavalent inorganic arsenic was introduced by intravenous, intratracheal, gastrointestinal, and skin application in doses 0.1 to 4.0 mg/kg in rats. Isotopic technics were applied by use of As(74). It was found that the dynamics of arsenic distribution in the body as well as the kinetics of its elimination in urine and feces varies very substantially, depending on the mode of administration. Intravenous administration of As causes immediate appearance of arsenic in most tissues and a slow decrease of its concentrations in time. Similar situations could be observed with intratracheal dosing, because arsenic is very rapidly absorbed from the site of administration. Concentration in tissues increases more slowly after gastrointestinal resorption. Skin application causes first the accumulation of arsenic in the skin and next continuous, slow transport from the skin into the blood stream. The rate of skin resorption was 1.14-33.1 mug/cm(2)-hr for 0.01-0.2M concentrations. The red blood cell level of arsenic is very substantial and does not change with time, which indicates the accumulation of arsenic in this tissue. The elimination of arsenic occurred chiefly in urine and feces, but the urine/feces ratio changed very substantially, depending on the route of administration. The kinetics of arsenic elimination in urine was multiphasic, being three-phase in case of intravenous and intratracheal administration and two-phase after gavage and skin resorption. After intravenous administration of As, the half-times of elimination were 2.5, 10, and 690 hr, respectively. Administration of selenium salts during the slow phase increased the rate of arsenic elimination. The straight-line relations found between the absorbed dose of arsenic and its blood or urine concentrations could serve as baselines for exposure tests for humans.

Administration, Oral↗
PubMed1977

Emissions of arsenic in Sweden and their reduction.

The role of arsenic in Sweden is generally described, including raw materials, exports/imports, products, consumption, etc. An attempt was also made to estimate the transport of arsenic in Sweden. The quantities of arsenic in raw materials, the emissions of arsenic from such processes as copper smelters and chemical industries, and the amounts of products containing arsenic were calculated. The studies show that a copper smelter is the main user of arsenical materials, the very largest emitting source and also the plant which manufacturers most arsenic products. A summary of measurements of arsenic in air, water and soil in Sweden has also been made. The concentrations near a smelter, in the Baltic, in cities and in "clean-air areas" are given. The efforts made to date to reduce the emissions of arsenic and the measures planned for the next few years are described. A reduction has already been achieved and a further rather large decrease will come, especially in arsenic levels in water. The possibilities of minimizing the use of materials and products containing arsenic is also discussed.

Air↗
PubMed1994

Bioavailability of inorganic arsenic from bog ore-containing soil in the dog.

In some parts of The Netherlands, bog ore-containing soils predominate, which have natural arsenic levels that exceed, by a factor of 10, existing standards for maximum allowable levels of inorganic arsenic in soil. These standards are based on the assumption that in humans the bioavailability of arsenic from ingested soil is equal to that from an aqueous solution. In view of the regulatory problem that the arsenic levels of these soils present, we questioned the validity of this assumption. To obtain a more realistic estimate, the bioavailability of inorganic arsenic from soil in a suitable animal model was studied. In this report, a study performed in six dogs in a two-way cross-over design is presented. The dogs received orally, in random order, arsenic both as an intravenous solution and as arsenic-containing soil. During a 120-hr period after administration urine was collected in 24-hr fractions. Levels of arsenic were determined using a method of wet digestion, isolation and complexation of arsine, followed by molecule absorption spectrometry. Within 120 hr after intravenous administration, 88 +/- 16% of the dose was excreted renally. After oral administration of arsenic-containing soil, only 7.0 +/- 1.5% was excreted renally. From the urinary excretion data for these two routes of administration, the calculated bioavailability of inorganic arsenic from soil was 8.3 +/- 2.0%. The results from this study demonstrate the need to reconsider the present risk assessment for arsenic in soil.

Animals↗
PubMed2006

Combined administration of N-acetylcysteine and monoisoamyl DMSA on tissue oxidative stress during arsenic chelation therapy.

The present study deals with the therapeutic potential of combined administration of N-acetylcysteine (NAC) along with monoisoamyl DMSA (MiADMSA) against chronic arsenic poisoning in guinea pigs. Animal were exposed to 50 ppm arsenic in drinking water for 8 mo and subsequently treated for 5 consecutive days with 100 mg/kg NAC (orally) and MiADMSA (intraperitoneally), individually or in combination (50 mg/kg each). Arsenic exposure produced a significant depletion of blood delta- aminolevulinic acid dehydrate (ALAD) activity, increased the blood zinc protoporphyrin (ZPP) level, and reduced blood and liver glutathione (GSH) levels in guinea pigs. Hepatic oxidized glutathione (GSSG) and thiobarbituric acid reactive substance (TBARS) levels showed a marked increase, whereas hepatic alkaline phosphatase (ALP) activity decreased and acid phosphatase (ACP) activity increased on arsenic exposure. Significant depletion of liver transaminase activities on arsenic exposure suggests organ injury. Administration of MiADMSA, alone and in combination with NAC after arsenic exposure, was able to significantly enhance hepatic GSH and to reduce GSSG and TBARS levels compared to the arsenic control. Biochemical variables indicative of liver injury generally remained insensitive to any of these treatments. The recoveries in parameters indicative of oxidative stress were more marked in guinea pigs treated with combined administration of NAC and MiADMSA than monotherapy. Interestingly, there was a more pronounced depletion of arsenic from blood and tissues after combined treatment with NAC plus MiADMSA than MiADMSA. Blood and tissues copper, zinc, iron, and calcium concentrations showed a significant increase after arsenic exposure, which showed improvement, particularly after combined administration of MiADMSA and NAC. Based on these data, a proposal can be made that greater effectiveness in chelation treatment against chronic arsenic poisoning (i.e., turnover in the oxidative stress and removed of arsenic from the system) could be achieved by combined administration of an antioxidant (preferably having a thiol moiety) with MiADMSA.

Acetylcysteine↗
PubMed2001

[Aluminum hydroxide hydrogel to remove arsenic from water].

OBJECTIVE: To describe the making of and the preliminary results from an aluminum hydroxide hydrogel that, when added directly to water, can totally eliminate arsenic, regardless of the nature of the water and the oxidation state of the metalloid. METHODS: The raw materials used to make the aluminum hydroxide hydrogel were: hydrated aluminum sulfate (which is used to make water safe for drinking), calcium hypochlorite in powder form, ammonium hydroxide, and distilled water (when done at the laboratory scale), and water from inverse osmosis of the same or better quality than the distilled water (when done at a pilot scale). Quality control for the finished product consisted of determining its ability to adsorb arsenic and performing bacteriological tests to demonstrate its sterility. The product was used with water samples to which arsenic had been added in the laboratory and with water samples from the province of Tucumán, Argentina, with naturally occurring arsenic. To analyze the arsenic in the water the colorimetric silver diethyldithiocarbamate method was used. RESULTS: Using the hydrogel greatly reduced the amount of arsenic. Treating both the natural and laboratory-produced arsenical waters yielded arsenic concentrations under the limit (0.01 parts per million) that was detectable with the analytical method used. The bacteriological tests of the finished product indicated there were no viable bacteria. CONCLUSIONS: Using the aluminum hydroxide hydrogel produced the desired reduction in the arsenic concentration in the water. This method for removing arsenic is inexpensive and easy to use in scattered rural populations in areas having high arsenic levels and lacking drinkable water, as well as an adequate sanitary and electric-power infrastructure.

Aluminum Hydroxide↗
PubMed2004

Consequences of acute and chronic exposure to arsenic in children.

Arsenic is a toxic chemical and may cause adverse health effects in children and adults. It is known to affect the nervous, gastrointestinal, and hematological systems and cause skin and internal cancers in people exposed to levels greater than 300 ppb in their drinking water. For most people, the major exposure to arsenic comes from food (8 to 14 microg inorganic arsenic per day), but when the arsenic level in water is elevated, drinking water becomes the predominant source of exposure. Because it is very difficult to limit arsenic exposure from food, it would be wise to limit arsenic exposure from those more controllable sources. Pediatricians should ascertain the levels of arsenic in drinking water of patients with high arsenic levels, using the supplier or, in the case of private wells, a professional water-testing laboratory assay. The Safe Drinking Water Act does not cover private wells or those water systems with less than 15 hook-ups or those that serve less than 25 people. Pediatricians should instruct parents to use prepared baby formulas or prepare them using water with the arsenic removed and to curtail playing time for younger children in places that have sand containing large amounts of arsenic. Such procedures will limit arsenic exposure to a minimum.

Arsenic↗
PubMed2002

Arsenic metabolites in human urine after ingestion of an arsenosugar.

BACKGROUND: Arsenic-containing carbohydrates (arsenosugars) are common constituents of marine algae, including those species used as human food. The toxicology of these compounds has not been fully evaluated. METHODS: Arsenic metabolites in human urine were monitored over a 4-day period after ingestion of a synthetic specimen of arsenosugar. The metabolites were determined by HPLC-inductively coupled plasma mass spectrometry, and structural assignments were confirmed with liquid chromatography-electrospray ionization mass spectrometry. RESULTS: Approximately 80% of the total ingested arsenic was excreted in the urine during the 4 days of the experiment. There was a lag-period of approximately 13 h before substantial quantities of arsenic appeared in the urine, and the excretion rate peaked between 22 and 31 h. At least 12 arsenic metabolites were detected, only 3 of which could be positively identified. Dimethylarsinate (DMA) was the major metabolite, constituting 67% of the total arsenicals excreted. A new urinary arsenic metabolite, dimethylarsinoylethanol, represented 5% of the total arsenicals, whereas trimethylarsine oxide was present as a trace (0.5%) constituent. One other significant metabolite cochromatographed with a reduced DMA standard, and hence was possibly dimethylarsinous acid. The second most abundant metabolite in the urine (20% of the total arsenic) remained unidentified, whereas the rest of the excreted arsenic was made up of several trace metabolites and small amounts of unchanged arsenosugar. CONCLUSIONS: Arsenosugars are biotransformed by humans to at least 12 arsenic metabolites, the toxicologies of which are currently unknown.

Arsenates↗
PubMed2002

Arsenic-mediated cellular signal transduction, transcription factor activation, and aberrant gene expression: implications in carcinogenesis.

Arsenic is a common environmental and occupational pollutant and a well-known human carcinogen that causes cancers in many human organs. The exact molecular mechanisms of arsenic carcinogenesis, however, are not well understood. It is generally acknowledged that arsenic does not act via a classic genotoxic or mutagenic mechanism, because it is not a direct mutagen. On the other hand, a growing amount of evidence has shown that arsenic shares many properties with tumor promoters by inducing intracellular signal transduction, activating transcription factors, and changing the expression of genes that are involved in promoting cell growth, proliferation, and malignant transformation. It is postulated that arsenic-induced mitogen-activated protein kinases (MAPKs) signal transduction, which leads to activation of transcription factors such as activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB) (which in turn alter gene expression), is associated with the carcinogenicity of arsenic. In this article, we review the recent findings in arsenic-induced MAPKs, AP-1 and NF-kappaB activation, and aberrant gene expression; their implications in arsenic carcinogenesis are discussed. The elucidation of arsenic-induced signal transduction pathways that lead to aberrant gene expression involved in the arsenic-triggered malignant transformation could help to identify novel molecular targets for the treatment of human cancers resulting from arsenic exposure.

Arsenic↗
PubMed2003

Arsenic contamination in parts of Yamuna sub-basin, West Bengal.

Arsenic rarely occurs in free state and is generally found in combination with Sulphur, Oxygen and Iron. In the environment, Arsenic occurs as a result of several inputs that contain this element in organic and inorganic forms. Arsenic is present in Coal, Lead, Zinc, Gold and Copper ores in the form of several minerals viz. Arsenopyrite (FeAsS), Orpiment (As2S3), Realgar (AsS), Arsenolite (As2O3) and Lollingite (FeAs2). The commonly existing species in groundwater are in two forms viz. Arsenite [As(III)] which is the reduced state of inorganic Arsenic and Arsenate [As(V)], which is the oxidized state of inorganic Arsenic, The As(III) form is more mobile and toxic for living organisms. Recently, the symptoms of chronic arsenic poisoning have been observed in many parts of West Bengal (India) and Bangladesh. In the present study, an integrated evaluation of hydrogeology and hydrochemistry has been carried out by processing the available data of Yamuna sub-basin (Part of Nadia and North 24 Parganas district) of West Bengal in order to understand the possible reason of arsenic pollution in the ground water. Arsenic has generally been observed in higher concentration in shallow aquifer. Northwestern region of the study area has been observed to be the most effected with premonsoon periods exhibiting higher concentration. Transmissivity values have been observed to vary inversely with arsenic concentrations. Arsenic values have not indicated any well defined association with many other constituents. Arsenic buildup could also not be conclusively related to lowering of ground water table of the study area.

Arsenic↗