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PubMed2003

Arsenic species contents at aquaculture farm and in farmed mouthbreeder (Oreochromis mossambicus) in blackfoot disease hyperendemic areas.

A study was conducted to measure the arsenic species in farmed mouthbreeder (Oreochromis mossambicus) and culture ponds in water in blackfoot disease (BFD) hyperendemic areas in Taiwan. The relationships between arsenic species of aquaculture ponds and farmed fish were also explored. Biota samples were extracted with methanol/water (1/1, v/v) using a Soxhlet extraction apparatus. The concentrations of arsenite As (III), arsenate As (V), monomethylarsonic acid (MMA), and dimethylarsinic acid (DMA) of extracts were measured by high-performance liquid chromatography (HPLC) linked to a hydride generator and atomic absorption spectrometry (HG-AAS). Moreover, arsenobetaine (AB) was analyzed by HPLC linked to ultra violet (UV) and HG-AAS. Concentrations of arsenic species were determined in 68 mouthbreeder (O. mossambicus) samples and 21 culture ponds from Putai and Yichu Townships of Chiayi County and Hsuehchia and Peimen Townships of Tainan County. The mean arsenic levels of culture ponds in Putai, Yichu, Hsuehchia, and Peimen were 75.8, 15.1, 14.4, and 221.0 microg/l, respectively. The water of culture ponds was dominated by As (V). The inorganic arsenic percentage of fish (7.4%) was higher than that reported by other seafood surveys. Except for the MMA and As (III) levels, As (V), DMA, AB, and total arsenic levels in fish significantly increased with inorganic and total arsenic concentrations of the pond water. Inorganic arsenic species are more toxic than methyl arsenic species. Therefore the effect of inorganic arsenic species might result in a greater number of adverse health effects to the general public. It is of importance to evaluate the inorganic arsenic levels of farmed seafood in arsenic-contaminated areas.

Agriculture↗
PubMed1990

[Effect of S-adenosylmethionine on methylation of inorganic arsenic].

We studied the role of S-adenosylmethionine (SAM) as a methyl group donor in the methylation of inorganic arsenic in mammalians. The SAM and S-adenosylhomocysteine (SAH) levels in the livers of untreated hamsters were 74.3 +/- 8.2 and 40.0 +/- 6.4 nmol/g, respectively. The SAM level was 63.9 +/- 6.5 nmol/g following oral administration of 1.5 mg/kg of arsenic trioxide, which was 14% lower than the control level (t-test, p less than 0.05). This fall of the SAM level in the liver presumably derived from the SAM having acted as a methyl group donor. Oral administration of 1.5 mg/kg of arsenic trioxide once only to hamsters pretreated intraperitoneally with 2.0 mg/kg of SAM once only gave the following arsenic levels in the liver and urine. The dimethylated arsenic (DMA) levels in the livers of hamsters treated with SAM plus arsenic trioxide were significantly high, that is, 2 times as high as the control value at 6 hours, and 1.5 times as high as the control value at 24 hours after the administration of arsenic trioxide. The urinary DMA excretion rate was significantly higher, that is, higher by 36%, than the control value. The urinary DMA excretion rate following pretreatment with SAM was not dose-dependent. Pretreatment with methionine failed to exert any significant acceleratory effect on the methylation of arsenic trioxide. The decreasing pattern of the SAM level in the liver following administration of arsenic trioxide and the DMA behavior in the liver and urine following administration of SAM and arsenic trioxide revealed that SAM accelerated the methylation of inorganic arsenic. In other words, it appeared that SAM could be a very potent methyl group donor to inorganic arsenic.

Animals↗
PubMed2003

Difference in uptake and toxicity of trivalent and pentavalent inorganic arsenic in rat heart microvessel endothelial cells.

Intake of inorganic arsenic is known to cause vascular diseases as well as skin lesions and cancer in humans. We investigated the differences in cytotoxicity, uptake rate of arsenic, and gene expression of antioxidative enzymes between arsenite (As(3+))- and arsenate (As(5+))-exposed rat heart microvessel endothelial cells. As(3+) was more cytotoxic than As(5+), and LC(50) values were calculated to be 36 and 220 micro M, respectively. As(3+) (1-25 micro M) increased mRNA levels of antioxidant enzymes such as heme oxygenase-1 (HO-1), thioredoxin peroxidase 2, NADPH dehydrogenase, and glutathione S-transferase P subunit. HO-1 mRNA levels showed the most remarkable increase in response to As(3+). cDNA microarray analysis indicated that there was no prominent difference in arsenic-induced transcriptional changes between As(3+)- and As(5+)-exposed cells, when the cells were exposed to one-fourth the LC(50) concentration of arsenic (9 and 55 micro M for As(3+) and As(5+), respectively). N-acetyl- l-cysteine (NAC) reduced both the cytotoxicity of inorganic arsenic and the HO-1 mRNA level, and buthionine sulfoximine enhanced cytotoxicity of inorganic arsenic. As(3+) was taken up by the endothelial cells 6-7 times faster than As(5+), and the presence of NAC in the culture medium did not change the uptake rate of As(3+). These results suggest that the effects of NAC on arsenic-induced cytotoxicity and oxidative stress were due to the antioxidative role of non-protein thiols and not to chelation of arsenic in the culture medium. The difference in cellular uptake of arsenic between As(3+) and As(5+) appeared not to be due to the ionic charge on arsenic (at physiological pH, trivalent arsenic is neutral whereas pentavalent arsenic is negatively charged). These results suggest that the higher toxicity of As(3+) compared with that of As(5+) is probably due to the faster uptake of As(3+) by endothelial cells, and inorganic arsenic exerts its toxicity at least in part via intracellular oxidative stress.

Acetylcysteine↗
PubMed2003

Speciation of arsenic in water, sediment, and plants of the Moira watershed, Canada, using HPLC coupled to high resolution ICP-MS.

High-performance liquid chromatography (HPLC) coupled with high-resolution sector field ICP-MS was applied to the speciation of arsenic in environmental samples collected from the Moira watershed, Ontario, Canada. Arsenic contamination in Moira River and Moira Lake from historic gold mine operations is of increasing environmental concern to the local community. In this study, the current arsenic contamination status in water, sediment, and plants was investigated. Elevated levels of arsenic in the surface water of up to 75 ng mL(-1) in Moira River and 50 ng mL(-1) in Moira Lake were detected, 98% of which was present as arsenate. High concentrations of arsenic (>300 ng mL(-1)), mainly present as arsenite, were detected in sediment porewaters. A sediment profile of As from the West basin of Moira Lake showed lower As concentrations compared with data from the 1990s. An optimized extraction procedure using a phosphoric acid-ascorbic acid mixture demonstrated that an unknown "As-complex" which may consist of As, sulfide and organic matter is potentially responsible for the release of arsenite from the sediment to the overlying water column. Arsenic concentrations in plant samples ranged from 2.6 to 117 mg kg(-1), dry weight. Accumulation of arsenic was observed in submerged plants collected from Moira River and Moira Lake. Only a small part of the arsenic (6.3-16.1%) in the plants was extractable with methanol-water (9:1), and most of this arsenic (70-93%) was inorganic arsenic. A variety of organic arsenic compounds, including simple methylated compounds (methylarsonic acid and dimethylarsinic acid), trimethylarsine oxide, and tetramethylarsonium cation were detected at trace levels. No arsenobetaine and arsenocholine was found in any plant sample. An unknown compound, most probably an arsenosugar was detected in the two submerged plants, coontail ( Ceratophyllum demersum) and long-stemmed waterwort ( Elatine triandra). These submerged plants are constantly exposed to high arsenic concentrations in the surrounding water. Apparently, they are able to grow in this environment without invoking the same biochemical defence known from marine algae to detoxify inorganic arsenic. The detoxification mechanism of these plants remains unknown.

Journal Article↗
PubMed2006

Arsenic resistance and removal by marine and non-marine bacteria.

Arsenic resistance and removal was evaluated in nine bacterial strains of marine and non-marine origins. Of the strains tested, Marinomonas communis exhibited the second-highest arsenic resistance with median effective concentration (EC(50)) value of 510 mg As l(-1), and was capable of removing arsenic from culture medium amended with arsenate. Arsenic accumulation in cells amounted to 2290 microg As g(-1) (dry weight) when incubated on medium containing 5 mg As l(-1) of arsenate. More than half of the arsenic removed was related to metabolic activity: 45% of the arsenic was incorporated into the cytosol fraction and 10% was found in the lipid-bound fraction of the membrane, with the remaining arsenic considered to be adsorbed onto the cell surface. Potential arsenic resistance and removal were also examined in six marine and non-marine environmental water samples. Of the total bacterial colony counts, 28-100% of bacteria showed arsenic resistance. Some of the bacterial consortia, especially those from seawater enriched with arsenate, exhibited higher accumulated levels of arsenic than M. communis under the same condition. These results showed that arsenic resistant and/or accumulating bacteria are widespread in the aquatic environment, and that arsenic-accumulating bacteria such as M. communis are potential candidates for bioremediation of arsenic contaminated water.

Arsenates↗
PubMed2000

Arsenic contamination in wood mice (Apodemus sylvaticus) and bank voles (Clethrionomys glareolus) on abandoned mine sites in southwest Britain.

Arsenic can be highly toxic to mammals but there is relatively little information on its transfer to and uptake by free-living small mammals. The aim of this study was to determine whether intake and accumulation of arsenic by wild rodents living in arsenic-contaminated habitats reflected environmental levels of contamination and varied between species, sexes and age classes. Arsenic concentrations were measured in soil, litter, wood mice (Apodemus sylvaticus) and bank voles (Clethrionomys glareolus) from six sites which varied in the extent to which they were contaminated. Arsenic residues on the most contaminated sites were three and two orders of magnitude above background in soil and litter, respectively. Arsenic concentrations in the stomach contents, liver, kidney and whole body of small mammals reflected inter-site differences in environmental contamination. Wood mice and bank voles on the same sites had similar concentrations of arsenic in their stomach contents and accumulated comparable residues in the liver, kidney and whole body. Female bank voles, but not wood mice, had significantly higher stomach content and liver arsenic concentrations than males. Arsenic concentration in the stomach contents and body tissues did not vary with age class. The bioaccumulation factor (ratio of arsenic concentration in whole body to that in the diet) in wood mice was not significantly different to that in bank voles and was 0.69 for the two species combined, indicating that arsenic was not bioconcentrated in these rodents. Overall, this study has demonstrated that adult and juvenile wood mice and bank voles are exposed to and accumulate similar amounts of arsenic on arsenic-contaminated mine sites and that the extent of accumulation depends upon the level of habitat contamination.

Journal Article↗
PubMed1987

Study of factors influencing the in vivo methylation of inorganic arsenic in rats.

Previous studies have shown that several factors may influence the methylation of inorganic arsenic by rat liver in vitro (Buchet and Lauwerys, 1985). The present study attempts to assess the relevance of these observations in vivo. Like man, rat inactivates inorganic arsenic by methylation to monomethylarsonic (MMA) and dimethylarsinic (DMA) acids which are excreted in urine along with unchanged inorganic arsenic (Asi). The administration of S-adenosylmethionine alone or in association with reduced (GSH) or oxidized glutathione or acetylcysteine and the increase of hepatic GSH level by butylated hydroxytoluene pretreatment do not stimulate the urinary excretion of the methylated arsenic metabolites following a challenge dose of inorganic arsenic. Conversely a reduction of the hepatic GSH level by phorone pretreatment greatly modifies the metabolism of inorganic arsenic in vivo. A reduction exceeding 90% of the control value leads to a decreased urinary excretion of MMA and DMA and an increased urinary excretion of inorganic arsenic. This is also associated with an increased accumulation of inorganic arsenic in the liver. This suggests that a drastic reduction of GSH level in liver not only impairs the methylation of inorganic arsenic but also impairs its biliary excretion. When GSH depletion is less severe, the total amount of arsenic excreted in urine after a challenge dose of NaAsO2 is not significantly different from that found in unpretreated animals but the proportion of the three metabolic forms is different: MMA is reduced whereas Asi and DMA tend to increase. These changes resemble those found in patients with liver insufficiency (J.P. Buchet, A. Geubel, S. Pauwels, P. Mahieu, and R. Lauwerys (1984). The influence of liver disease on the methylation of arsenite in humans. Arch. Toxicol. 55, 151-154). Long-term pretreatment of rats with CCl4 slightly reduces the amount of MMA and DMA excreted in urine following a challenge dose of inorganic arsenic. This effect may result from a reduction of GSH transferase activity by CCl4. This study demonstrates the important role of liver GSH in the metabolism of inorganic arsenic in vivo.

Animals↗
PubMed2004

Mental health burden amongst inhabitants of an arsenic-affected area in Inner Mongolia, China.

Inner Mongolia, China, is an area with high levels of arsenic. The adverse health effects resulting from chronic arsenic exposure include skin keratosis, vascular diseases and cancers. However, the effects of arsenic exposure on mental health have not received much attention. The purpose of this study was to examine the effects of arsenic poisoning on the mental health of the inhabitants of an arsenic-affected area. We performed a cross-sectional study at two villages in Hetao Plain, Inner Mongolia. The populations of both villages were similar in age, sex, lifestyle, socioeconomic conditions, and geographic location. One hundred and thirty four (93.7%) of the 143 inhabitants in the arsenic-affected village and 36 (76.6%) of the 47 inhabitants in the arsenic-free village participated in the study. Subjects with a 30-item version of General Health Questionnaire score of 9 or more were defined as having symptoms of distress. The multiple logistic analyses showed that the mental health of the subjects in the arsenic-affected village was worse than in those in the arsenic-free village (OR=2.5, 95% CI=1.1-6.0). The effect of arsenic on mental health in arsenic-affected areas deserves further investigation. The mental health burden in arsenic-affected areas should be considered in the wider context of public and community health.

Adult↗
PubMed2004

The potential biological mechanisms of arsenic-induced diabetes mellitus.

Although epidemiologic studies carried out in Taiwan, Bangladesh, and Sweden have demonstrated a diabetogenic effect of arsenic, the mechanisms remain unclear and require further investigation. This paper reviewed the potential biological mechanisms of arsenic-induced diabetes mellitus based on the current knowledge of the biochemical properties of arsenic. Arsenate can substitute phosphate in the formation of adenosine triphosphate (ATP) and other phosphate intermediates involved in glucose metabolism, which could theoretically slow down the normal metabolism of glucose, interrupt the production of energy, and interfere with the ATP-dependent insulin secretion. However, the concentration of arsenate required for such reaction is high and not physiologically relevant, and these effects may only happen in acute intoxication and may not be effective in subjects chronically exposed to low-dose arsenic. On the other hand, arsenite has high affinity for sulfhydryl groups and thus can form covalent bonds with the disulfide bridges in the molecules of insulin, insulin receptors, glucose transporters (GLUTs), and enzymes involved in glucose metabolism (e.g., pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase). As a result, the normal functions of these molecules can be hampered. However, a direct effect on these molecules caused by arsenite at physiologically relevant concentrations seems unlikely. Recent evidence has shown that treatment of arsenite at lower and physiologically relevant concentrations can stimulate glucose transport, in contrary to an inhibitory effect exerted by phenylarsine oxide (PAO) or by higher doses of arsenite. Induction of oxidative stress and interferences in signal transduction or gene expression by arsenic or by its methylated metabolites are the most possible causes to arsenic-induced diabetes mellitus through mechanisms of induction of insulin resistance and beta cell dysfunction. Recent studies have shown that, in subjects with chronic arsenic exposure, oxidative stress is increased and the expression of tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) is upregulated. Both of these two cytokines have been well known for their effect on the induction of insulin resistance. Arsenite at physiologically relevant concentration also shows inhibitory effect on the expression of peroxisome proliferator-activated receptor gamma (PPARgamma), a nuclear hormone receptor important for activating insulin action. Oxidative stress has been suggested as a major pathogenic link to both insulin resistance and beta cell dysfunction through mechanisms involving activation of nuclear factor-kappaB (NF-kappaB), which is also activated by low levels of arsenic. Although without supportive data, superoxide production induced by arsenic exposure can theoretically impair insulin secretion by interaction with uncoupling protein 2 (UCP2), and oxidative stress can also cause amyloid formation in the pancreas, which could progressively destroy the insulin-secreting beta cells. Individual susceptibility with respect to genetics, nutritional status, health status, detoxification capability, interactions with other trace elements, and the existence of other well-recognized risk factors of diabetes mellitus can influence the toxicity of arsenic on organs involved in glucose metabolism and determine the progression of insulin resistance and impaired insulin secretion to a status of persistent hyperglycemia or diabetes mellitus. In conclusions, insulin resistance and beta cell dysfunction can be induced by chronic arsenic exposure. These defects may be responsible for arsenic-induced diabetes mellitus, but investigations are required to test this hypothesis.

Animals↗
PubMed2006

Screening high-fluoride and high-arsenic drinking waters and surveying endemic fluorosis and arsenism in Shaanxi province in western China.

The objectives of this study were to screen high-fluoride and high-arsenic drinking waters, to evaluate the effectiveness of fluoride-reducing projects and to assess the present condition of endemic fluorosis and arsenism in Shaanxi province in western China. For screening high-fluoride drinking waters, five water samples were collected from each selected village where dental fluorosis patients were detected in 8-12 year-old children. For evaluating the effectiveness of fluoride-reducing projects, four water samples were collected from each project at end-user level. Fluoride concentrations in water samples were measured by fluoride-selective electrode method or spectrophotometry. Dental fluorosis in children aging 8-12 years was examined according to Horowitz's Tooth Surface Index of Fluorosis. Skeletal fluorosis in adults was detected clinically and radiologically according to Chinese Criteria of Clinical Diagnosis of Skeletal Fluorosis. For screening high-arsenic waters, 20 water samples were collected from each village which was selected from areas characterized by the geographic features to induce high-arsenic underground water, i.e., alluvial plains, ore mining or smelting areas, geothermal artesians, and thermal springs. Arsenic concentrations in water samples were determined by spectrophotometry or arsine generation atomic fluorospectrophotometry. Arsenism in adults aging 40-89 years was examined in villages with arsenic concentrations in drinking water above 0.05 mg/l according to Chinese Criteria for Classification of Endemic Arsenism Areas and Clinical Diagnoses of Endemic Arsenism. The results showed that the fluoride level of 7144 water samples was 1.17 +/- 0.93 mg/l. There were 3396 (47.6%) high-fluoride waters (fluoride level was above 1.0 mg/l) distributing in 786 (45.1%) villages, where about 0.8 million (50.0%) people inhabited. Additionally, the 1315 fluoride-reducing projects were studied. The fluoride level of the projects was 2.79 +/- 1.09 and 0.98 +/- 0.47 mg/l before and after building the projects, which remained at relatively lower level (1.03 +/- 0.47 mg/l). But there were still 58.0% of the projects providing drinking waters with fluoride concentrations beyond 1.0mg/l. The rates of dental fluorosis and skeletal fluorosis were 38.2% and 11.8%, respectively. The arsenic level of 1732 water samples was 0.010 +/- 0.082 mg/l. There were 174 (14.9%) high-arsenic waters (arsenic level was above 0.010 mg/l) being detected, distributing in 41 (38.7%) villages. The arsenic level in 53 (4.5%) water samples was beyond 0.025 mg/l. There were 3 villages with arsenic level in drinking water beyond Chinese National Permissible Limits (0.050 mg/l), and the prevalence rate of arsenism reached 37.0% in these three villages, 3.7%, 22.2%, and 11.1% of subjects suffering from mild, moderate, and severe arsenism, respectively. Conclusively, the wide distribution of high-fluoride drinking waters contributes to the prevalence of dental and skeletal fluorosis in Shaanxi province and the quality of fluoride-reducing projects should be further improved. Ore mining and smelting induces high-arsenic drinking waters, resulting in arsenism prevalence in Shang-luo city. Proper measures should be taken to deal with water pollution in the ore mining and smelting areas in order to solve the high-arsenic water problem in Shaanxi province.

Adult↗
PubMed2003

DNA repair gene XPD and susceptibility to arsenic-induced hyperkeratosis.

Chronic exposure to inorganic arsenic is known to cause non-melanocytic skin and internal cancers in humans. An estimated 50-70 million people in Bangladesh have been chronically exposed to arsenic from drinking water and are at risk of skin and other cancers. We undertook the first study to examine whether genetic susceptibility, as determined by the codon 751 SNP (A-->C) of the DNA repair gene XPD, influences the risk of arsenic-induced hyperkeratotic skin lesions, precursors of skin cancer, in a case-control study of 29 hyperkeratosis cases and 105 healthy controls from the same community in an area of Bangladesh. As expected, there was a monotonic increase in risk of hyperkeratosis in relation to urinary arsenic measures but the XPD genotype was not independently associated with the risk. However, the increase in hyperkeratosis risk in relation to urinary arsenic measures genotype was borderline significant for urinary total arsenic (P for trend=0.06) and statistically significant for urinary creatinine adjusted arsenic (P for trend=0.01) among subjects with the XPD A allele (AA) but not among subjects with the other XPD genotypes. Among AA carriers, the risk for the highest arsenic exposed group compared with the lowest was more than 7-fold for urinary total arsenic and about 11-fold for urinary creatinine adjusted arsenic. In conclusion, our findings suggest that the DNA repair gene XPD may influence the risk of arsenic-induced premalignant hyperkeratotic skin lesions. Future larger studies are needed to confirm this novel finding and investigate how combinations of different candidate genes and/or other host and environmental factors may influence the risk of arsenic induced skin and other cancers.

Adult↗
PubMed2000

Decreased serum concentrations of nitric oxide metabolites among Chinese in an endemic area of chronic arsenic poisoning in inner Mongolia.

Prolonged exposure to arsenic results in peripheral and cardiovascular manifestations, as does impaired production of endothelial nitric oxide (NO). In vitro studies have indicated that endothelial cells undergo damage by arsenic. However, no information has been available on the relationship between NO synthesis and chronic arsenic poisoning in humans. The present study was designed to reveal this question. The subjects were 33 habitants who continued to drink well water containing high concentrations of inorganic arsenic (mean value = 0.41 microg/ml) for about 18 years in Inner Mongolia, China, and 10 other people who lived in this area but exposed to minimal concentrations of arsenic (mean value = 0.02 microg/ml) were employed as controls. Mean blood concentration of total arsenic was six times higher in exposed subjects than controls; 42.1 vs. 7.3 ng/ml, p <.001. Mean serum concentration of nitrite/nitrate, stable metabolites of endogenous NO, was lower in arsenic-exposed subjects than in controls: 24.7 vs. 51.6 microM, p<.001. In total samples, an inverse correlation with serum nitrite/nitrate levels was strong for blood inorganic arsenic (r = -0.52, p <.001) and less strong for its metabolites, monomethyl arsenic (r = -0.45, p<.005) and dimethyl arsenic (r = -0.37, p<.05). Furthermore, serum nitrite/nitrate concentration was significantly correlated with nonprotein sulfhydryl level in whole blood (r = 0.58, p<.001). In an in vitro study, we demonstrated that inorganic arsenite or arsenate suppresses the activity of endothelial NO synthase in human umbilical vein endothelial cells. These results suggest that long-term exposure to arsenic by drinking well water possibly reduces NO production in endothelial cells, resulting in a decrease in reduced nitrite/nitrate concentrations. Peripheral vascular disorders caused by arsenic may be attributable in part to impairment of NO production in vivo.

Adolescent↗
PubMed2005

Arsenic speciation in farmed Hungarian freshwater fish.

Arsenic speciation analysis was carried out on freshwater farmed fish collected from an area with elevated groundwater arsenic concentrations in Hungary as well as from outside of the area (control samples). The arsenic species were determined by high-performance liquid chromatography-inductively coupled plasma mass spectrometry on methanol extracts of the muscle tissue from the fish. Catfish (Claries gariepinus) were raised in geothermal water where the average total arsenic concentrations were 167 (contaminated sites) and 15.1 ng As mL(-1) (control); they were all fed an artificial diet containing 2880 microg As kg(-1) total arsenic, mostly present as arsenobetaine. In the catfish, the accumulated total arsenic (2510-4720 microg As kg(-1)) was found mostly in the form of arsenobetaine suggesting that uptake of arsenic was dominated by their diet. Carp (Cyprinus carpio) were cultured in surface lakes with no significant arsenic pollution and had total arsenic concentrations ranging from 62 to 363 microg As kg(-1). The arsenic species found in the carp extracts differed markedly from those in the catfish in that no arsenobetaine was detected. Most samples of carp from the investigated sites contained low concentrations of As(III) (arsenite), As(V) (arsenate), MA (methylarsonate), and DMA (dimethylarsinate), and no other compounds were detected. The four individuals from the control site, however, all contained appreciable levels of oxo-arsenosugar-glycerol and oxo-arsenosugar-phosphate. Indeed, the oxo-arsenosugar-phosphate dominated the speciation pattern for these carp contributing about 75% of the sum of species. The contrast between these two freshwater aquaculture species regarding total arsenic and arsenic species has relevant toxicological aspects in terms of food safety.

Animals↗
PubMed2003

High arsenic groundwater: mobilization, metabolism and mitigation--an overview in the Bengal Delta Plain.

The widespread occurrence of high inorganic arsenic in natural waters is attributed to human carcinogen and is identified as a major global public health issue. The scale of the problem in terms of population exposure (36 million) and geographical area coverage (173 x 10(3) Km2) to high arsenic contaminated groundwater (50-3200 microgL(-1)) compared to the National drinking water standard (50 microgL(-1)) and WHO recommended provisional limit (10 microgL(-1)) is greatest in the Holocene alluvium and deltaic aquifers of the Bengal Delta Plain (Bangladesh and West Bengal, India). This large-scale 'natural' high arsenic groundwater poses a great threat to human health via drinking water. Mobilization, metabolism and mitigation issues of high arsenic groundwater are complex and need holistic approach for sustainable development of the resource. Mobilization depends on the redox geochemistry of arsenic that plays a vital role in the release and subsequent transport of arsenic in groundwater. Metabolism narrates the biological response vis-à-vis clinical manifestations of arsenic due to various chemical and biological factors. Mitigation includes alternative source for safe drinking water supply. Drinking water quality regulatory standards as well as guidelines are yet to cover risk assessments for such metal toxicity. Lowering of the ingested inorganic arsenic level and introduction of newer treatment options (implementation of laterite, the natural material) to ensure safe water supply (arsenic free and/or low arsenic within permissible limit) are the urgent need to safe guard the mass arsenic poisoning and internal arsenic related health problems.

Arsenic↗
PubMed2001

Application of cDNA microarray to the study of arsenic-induced liver diseases in the population of Guizhou, China.

Arsenic is an environmental toxicant and a human carcinogen. Epidemiology studies link human arsenic exposure to various diseases and cancers, including liver diseases and hepatocellular carcinoma. However, the molecular mechanisms for arsenic toxicity and carcinogenicity are poorly understood. To better understand these mechanisms, we used the human cancer cDNA expression array to profile aberrant gene expression in arsenic-exposed populations in Guizhou, China. The selected patients had a history of exposure to environmental arsenic for at least 6-10 years, and had arsenic-induced skin lesions and hepatomegaly. Samples were obtained by liver needle biopsy. Histology showed degenerative liver lesions, such as chronic inflammation, vacuolation, and focal necrosis. The University of North Carolina Hospitals provided normal human liver tissues from surgical resection or rejected transplants. Microarray was performed with total RNA from liver samples, and signal intensities were analyzed with AtlasImage software and normalized with 9 housekeeping genes. Means and SEM were calculated for statistical analysis. Approximately 60 genes (10%) were differentially expressed in arsenic-exposed human livers compared to controls. The differentially expressed genes included those involved in cell-cycle regulation, apoptosis, DNA damage response, and intermediate filaments. The observed gene alterations appear to be reflective of hepatic degenerative lesions seen in the arsenic-exposed patients. This array analysis revealed important patterns of aberrant gene expression occurring with arsenic exposure in human livers. Aberrant expressions of several genes were consistent with the results of array analysis of chronic arsenic-exposed mouse livers and chronic arsenic-transformed rat liver cells. Clearly, a variety of gene expression changes may play an integral role in arsenic hepatotoxicity and possibly carcinogenesis.

Arsenic↗
PubMed2005

Dietary intake and arsenic methylation in a U.S. population.

Millions of people worldwide are exposed to arsenic-contaminated drinking water, and ingestion of inorganic arsenic (InAs) has been associated with increased risks of cancer. The primary metabolic pathway of ingested InAs is methylation to monomethyl arsenic (MMA) and dimethyl arsenic (DMA). However, people vary greatly in the degree to which they methylate InAs, and recent evidence suggests that those who excrete high proportions of ingested arsenic as MMA are more susceptible than others to arsenic-caused cancer. To date, little is known about the factors that determine interindividual differences in arsenic methylation. In this study, we assessed the effect of diet on arsenic metabolism by measuring dietary intakes and urinary arsenic methylation patterns in 87 subjects from two arsenic-exposed regions in the western United States. Subjects in the lower quartile of protein intake excreted a higher proportion of ingested InAs as MMA (14.6 vs. 11.6%; p = 0.01) and a lower proportion as DMA (72.3 vs. 77.0%; p = 0.01) than did subjects in the upper quartile of protein intake. Subjects in the lower quartile of iron, zinc, and niacin intake also had higher urinary percent MMA and lower percent DMA levels than did subjects with higher intakes of these nutrients. These associations were also seen in multivariate regression analyses adjusted for age, sex, smoking, and total urinary arsenic. Given the previously reported links between high percent MMA and increased cancer risks, these findings are consistent with the theory that people with diets deficient in protein and other nutrients are more susceptible than others to arsenic-caused cancer.

Adult↗
PubMed1979

Arsenic exposure in multiple environmental media in children near a smelter.

A nationwide survey of heavy-metal exposure in children living near primary nonferrous metal smelters demonstrated high urine arsenic levels in children living near a copper smelter in Ajo, Arizona. Airborne smelter emissions and drinking water were the apparent sources of exposure. To determine whether increased arsenic absorption had produced adverse health effects, we conducted an evaluation of 132 Ajo children 5 to 18 years old and compared results with those of 47 children from a comparison town with low arsenic exposure. Environmental testing showed that Ajo's municipal water supply contained arsenic in concentrations of 0.09 mg/l (the EPA standard is 0.05 mg/l); arsenic concentrations in dust averaged 342.2 microgram/g. Urine arsenic levels in Ajo children correlated positively with amount of tap-water consumed (r = .32, p less than. 0002) and with distance of residence from the smelter (r = .20, p less than .02). Tap-water drinkers had significantly higher urine arsenic levels than bottled water drinkers (t = 4.21 p less than .001). Mean urine arsenic levels were significantly higher for children in Ajo (4.75 microgram/100 ml) than for children in the comparison town (1.17 microgram/100 ml). Hair arsenic levels correlated poorly with arsenic exposure. Despite the study population's chronic exposure to elevated environmental levels of arsenic, no clinical or hematologic abnormalities attributable to arsenic were found.

Adolescent↗
PubMed2006

Arsenic compounds in the treatment of multiple myeloma: a new role for a historical remedy.

Arsenic compounds have been used since ancient times to treat a wide variety of ailments. Although the use of arsenic to treat hematologic cancers has been documented since the 19th century, widespread use of arsenic compounds in patients with hematologic malignancies did not occur until the 1990s, when several groups in China reported impressive clinical response rates in patients with acute promyelocytic leukemia who had received arsenic trioxide. Subsequently, clinical studies conducted in the United States confirmed earlier reports, and arsenic trioxide was approved by the Food and Drug Administration for the treatment of relapsed/refractory acute promyelocytic leukemia. The use of arsenic compounds in the treatment of multiple myeloma (MM) is supported by the proposed mechanisms of action underlying the antitumor activity of arsenic and by preclinical studies showing antiproliferative and cytotoxic activities in cell culture and animal models. Moreover, clinical studies of arsenic compounds, particularly arsenic trioxide-based regimens, have shown that this drug is clinically active in patients with relapsed/refractory MM. Combination studies with other antimyeloma agents have shown evidence of synergy with arsenic trioxide. Furthermore, arsenic trioxide-based regimens in MM appear to be well tolerated, particularly with regard to cardiac toxicity. The activity and tolerability observed in clinical studies promise to make arsenic-based chemotherapy a viable treatment option for patients whose disease does not respond to or who cannot tolerate other chemotherapy regimens.

Antineoplastic Agents↗