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PubMed2003

Metabolism of arsenic by sheep chronically exposed to arsenosugars as a normal part of their diet. 1. Quantitative intake, uptake, and excretion.

Information on the effects of long-term organoarsenical consumption by mammals is limited despite the fact that foodstuffs, especially seafood, often contain organoarsenicals at very high concentrations. Here we evaluate the intake, uptake, and excretion (urine and feces) of arsenic by sheep that live on North Ronaldsay in the Orkney Islands and naturally consume large amounts of arsenosugars through their major food source-seaweed. The sheep eat a broad variety of seaweed species, and arsenic concentrations were determined in all the species observed eaten by the sheep (5.7-74.0 mg kg(-1) dry mass). Because of preference and availability, they feed mostly on the seaweed species found to contain the highest arsenic concentrations: Laminaria digitata and Laminaria hyperborea (74 +/- 4 mg kg(-1) dry mass). To quantify the arsenic intake by the sheep, a feeding experiment reflecting natural conditions as close as possible was set up. In the feeding trial, the average daily intake of arsenic by 12 ewes was 35 +/- 6 mg (97% of water-extractable arsenic was present as arsenosugars) gained from feeding on the two brown algae. To test the possible influence of microflora on the metabolism of arsenosugars, six of the sheep were adapted to feeding on grass for 5 months before the start of the trial (control sheep), and the remaining six sheep were kept on their normal seaweed diet (wild sheep). No significant difference in seaweed/arsenic intake and arsenic excretion was found between the two groups of sheep. The arsenic excreted in the feces represents 13 +/- 10% (n = 12) of the total consumed, and on the assumption of that, the average urinary excretion is estimated to 86%.The main arsenic metabolite excreted in urine was dimethylarsinic acid (DMA(V)) (60 +/- 22%) and minor amounts of dimethylarsinoylethanol (DMAE), methylarsonic acid (MA(V)),tetramethylarsonium ion (TMA+), and arsenate (As(V)) together with seven unknown arsenic compounds were also excreted. The urinary arsenic excretion pattern showed a lag period (>4 h) before significant quantities appeared in the urine, an excretion rate that peaked between 4 and 28 h after seaweed intake and a relatively slow half-life (17 h) after end of intake.

Animal Feed↗
PubMed1998

Arsenic species in drinking water, hair, fingernails, and urine of patients with blackfoot disease.

A large number of residents on the southwest coast of Taiwan suffer from an endemic peripheral vascular disease called blackfoot disease. Although the etiology has been investigated since 1958, the cause of blackfoot disease remains unknown. Certain substances contained in artesian well water have been implicated as causal factors, including arsenic as the predominant element. Data in this study demonstrated that in the well water collected from blackfoot disease regions of Taiwan there was a marked increase in total arsenic concentrations, with the predominant species being inorganic arsenical compounds. The concentrations of organic methyl arsenicals were present in minimal amounts. The excretion of total arsenic, inorganic arsenic, monomethylarsonic acid, and trimethylarsenic acid in the urine of patients afflicted with blackfoot disease was significantly higher than for control subjects. Further, in patients with blackfoot disease the concentrations of total arsenic and inorganic arsenic were markedly elevated in the hair and fingernails. Data suggest that blackfoot disease is associated with individuals ingesting well, water contaminated with arsenic primarily in the inorganic form and that hair, fingernails, or urine specimens serve as equally effective biomarkers of exposure. The fact that arsenic intoxication as manifested by blackfoot disease is still prevalent despite the stoppage of well-water consumption for two decades illustrates the persistent nature of arsenic action.

Aged↗
PubMed2003

Modulation of the arsenic effects on cytotoxicity, viability, and cell cycle in porcine endothelial cells by selenium.

The differential effects of arsenic compounds and the effect of selenium on arsenic-induced changes in cytotoxicity, viability, and cell cycle of porcine aorta endothelial cells (PAECs) were investigated. MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay indicated that arsenic trioxide (As(2)O(3)) and sodium arsenite (NaAsO(2)) showed similar cytotoxicity, whereas sodium arsenate (Na(2)HAsO(4)) did not show cytotoxicity in PAECs. As(2)O(3) and NaAsO(2) at 20 microM decreased PAEC viability, decreased G0/G1 phase, and increased apoptosis. An increased G2/M phase was observed in NaAsO(2)-treated PAECs, whereas an increase in secondary necrosis (late apoptosis) was observed in As(2)O(3)-treated PAECs. As(2)O(3)-induced apoptosis was associated with upregulation of p53 and caspase 3, whereas NaAsO(2)-induced apoptosis was associated with p53 upregulation. Sodium selenite (Na(2)SeO(3)) at 1 nM reduced 20 microM As(2)O(3)-induced cytotoxicity, but not apoptosis, at 24 h. Increased glutathione peroxidase (GPX) activity by Na(2)SeO(3) pretreatment in 20 microM As(2)O(3)-treated PAECs suggests that Na(2)SeO(3) modulates As(2)O(3)-induced cytoxicity by GPX modulation.

Animals↗
PubMed2004

Understanding arsenic carcinogenicity by the use of animal models.

Although numerous epidemiological studies have indicated that human arsenic exposure is associated with increased incidences of bladder, liver, skin, and lung cancers, limited attempts have been made to understand mechanisms of carcinogenicity using animal models. Dimethylarsinic acid (DMA), an organic arsenic compound, is a major metabolite of ingested inorganic arsenics in mammals. Recent in vitro studies have proven DMA to be a potent clastogenic agent, capable of inducing DNA damage including double strand breaks and cross-link formation. In our attempts to clarify DMA carcinogenicity, we have recently shown carcinogenic effects of DMA and its related metabolites using various experimental protocols in rats and mice: (1) a multi-organ promotion bioassay in rats; (2) a two-stage promotion bioassay by DMA of rat urinary bladder and liver carcinogenesis; (3) a 2-year carcinogenicity test of DMA in rats; (4) studies on the effects of DMA on lung carcinogenesis in rats; (5) promotion of skin carcinogenesis by DMA in keratin (K6)/ornithine decarboxylase (ODC) transgenic mice; (6) carcinogenicity of DMA in p53(+/-) knockout and Mmh/8-OXOG-DNA glycolase (OGG1) mutant mice; (7) promoting effects of DMA and related organic arsenicals in rat liver; (8) promoting effects of DMA and related organic arsenicals in a rat multi-organ carcinogenesis test; and (9) 2-year carcinogenicity tests of monomethylarsonic acid (MMA) and trimethylarsine oxide (TMAO) in rats. The results revealed that the adverse effects of arsenic occurred either by promoting and initiating carcinogenesis. These data, as covered in the present review, suggest that several mechanisms may be involved in arsenic carcinogenesis.

Animals↗
PubMed2002

A review of animal models for the study of arsenic carcinogenesis.

As inorganic arsenic is a proven human carcinogen, significant effort has been made in recent decades in an attempt to understand arsenic carcinogenesis using animal models, including rodents (rats and mice) and larger mammals such as beagles and monkeys. Transgenic animals were also used to test the carcinogenic effect of arsenicals, but until recently all models had failed to mimic satisfactorily the actual mechanism of arsenic carcinogenicity. However, within the past decade successful animal models have been developed using the most common strains of mice or rats. Thus dimethylarsinic acid (DMA), an organic arsenic compound which is the major metabolite of inorganic arsenicals in mammals, has been proven to be tumorigenic in such animals. Reports of successful cancer induction in animals by inorganic arsenic (arsenite and arsenate) have been rare, and most carcinogenetic studies have used organic arsenicals such as DMA combined with other tumor initiators. Although such experiments used high concentrations of arsenicals for the promotion of tumors, animal models using doses of arsenicals species closed to the exposure level of humans in endemic areas are obviously the most significant. Almost all researchers have used drinking water or food as the pathway for the development of animal model test systems in order to mimic chronic arsenic poisoning in humans; such pathways seem more likely to achieve desirable results.

Animals↗
PubMed1961

Study and application of molluscicides in Japan.

For several years after the First World War calcium oxide was the main compound used in the control of Oncomelania nosophora in Japan. This was generally replaced in 1944 by calcium cyanamide; since 1952 the prefectural authorities in areas of endemic bilharziasis have increasingly turned to the use of sodium pentachlorophenate as the molluscicide of choice. Applied at a rate of 5 g per m(2), this compound has been found to kill 70%-80% of snails per application.Laboratory and field experiments with calcium-arsenic compounds have been conducted in Japan and have indicated that these products have a relatively high molluscicidal effect; they have, however, not been used on a wide scale for snail control.

Animals↗
PubMed1987

The identification of arsenobetaine as the sole water-soluble arsenic constituent of the tail muscle of the western king prawn Penaeus latisulcatus.

1. Samples of tail muscle of the western king prawn, Penaeus latisulcatus collected from two locations were examined separately for the presence of arsenobetaine and other arsenic compounds. 2. For both samples the aqueous extract accounted for greater than 97% of the total arsenic. 3. The water-soluble arsenic was present as one compound only which was isolated and identified as arsenobetaine.

Animals↗
PubMed2000

[Effect of arsenic and its compounds on the circulatory system].

Arsenic is a metal which occurs widely in both occupational and physical environments. Therefore, its easy accessibility and high toxicity raise the question on whether arsenic, particularly in relatively small doses, can cause damage of relevant molecular, biochemical and clinical significance to the cardiovascular system. The present review is focused on the confirmed and potential mechanisms of arsenic effect on the function and structure of vascular endothelium (nitric oxide, peroxynitrite), its role in stimulating the oxidative species formation (hydroxyperoxide, superoxide and lipid peroxide formation), as well as in decreasing the antioxidative response (enzymes: superoxide dysmutase, catalase, glutation peroxidase), its cytotoxic effects, including immunotoxic properties, arsenic action in the signal transduction pathways network (kinases and DNA transcription factors), impact on cell proliferation, differentiation and apoptosis, not to mention its interference with DNA synthesis and repair processes. Apart from mechanisms of arsenic action, the article provides the up-to-date information on various cardiovascular diseases of the established or presumed arsenic origin.

Animals↗
PubMed1999

Hydrogeological investigation of ground water arsenic contamination in south Calcutta.

Typical clinical symptoms of acute arsenic poisoning have been detected in 1000 residents near a factory in P.N. Mitra Lane, Behala, South Calcutta, located in a thickly populated area manufacturing copper acetoarsenite (Paris-Green) an arsenical pesticide for the past 25 years. Soil around the effluent dumping point of the factory was exceptionally contaminated, with arsenic, copper and chromium concentrations of 20,100-35,500 mg kg-1, 33,900-51,100 mg kg-1 and 5300-5510 mg kg-1. Arsenic and copper concentrations in bore-hole soils collected up to a depth of 24.4 m at the effluent dumping point, decreased with depth. Arsenous acid, arsenic acid, methylarsonic acid (MA) and dimethylarsinic acid (DMA) were detected in bore-hole soils up to a depth of 1.37 m, after which only inorganic arsenical compounds were present. A positive correlation was established between arsenic and copper authenticated the Paris-Green waste disposal site as the source of contamination. Mechanism of ground water contamination from this disposal site had been probed by a systematic hydrogeological survey and the arsenic content of the tube-well waters in the surrounding areas. Hydraulic conductivity was maximum in the central part. The site for disposal of the effluent was a ditch located in the zone of discharge. Sparingly soluble Paris-Green cumulatively deposited in the waste disposal site is decomposed by micro-organisms to water-soluble forms and finally percolated to underground aquifers along with rain water through the discharge zone. The contaminant is currently moving towards WNW with ground water flow and the residents in the direction of encroaching contamination are insecure due to penetration of the contaminant.

Arsenic↗
PubMed2003

Treatment of relapsed acute promyelocytic leukemia.

By all-trans retinoic acid (ATRA) and chemotherapy over 70% of patients with newly diagnosed acute promyelocytic leukemia (APL) may be cured; 20-30% of patients still relapse and require salvage therapy. For relapsed or refractory APL, a standard treatment has not yet been defined. However, several effective drugs and approaches have been described. Treatment options for relapsed APL include chemotherapy regimens used in the treatment of relapsed acute myeloid leukemia usually combined with ATRA or of other differentiating agents such as liposomal ATRA or synthetic retinoids. Presently, allogeneic peripheral stem cell or bone marrow transplantation is the treatment of choice for younger patients who have a histocompatible donor, as it gives the chance of cure in second or further relapse. For patients without a donor or for those who are not suitable for allogeneic transplantation, autologous stem cell or bone marrow transplantation may offer at least the possibility of a prolongation of remission, if the harvested cells are negative in the RT-PCR of PML/RAR alpha. Arsenic compounds have a high antileukemic effectiveness on APL cells. Arsenic trioxide has recently been approved for relapsed or refractory APL. With this drug, complete hematologic remission rates of 80-92% and long-lasting molecular remissions were achieved in relapsed patients. For patients who do not qualify for these treatment options, monoclonal anti-CD33 antibodies may represent further treatment options.

Antineoplastic Agents↗
PubMed1981

A rapid method for the selective analysis of total urinary metabolites of inorganic arsenic.

Total urinary arsenic has traditionally been used for assessing occupational exposure to inorganic arsenic. However, dietary arsenic, especially from seafood, may greatly influence this value. This paper describes a fast and convenient method for routinely measuring the combined amount of inorganic arsenic, methylarsonic acid, and dimethylarsinic acid, which are the major urinary metabolites after exposure to inorganic arsenic. Organic arsenic compounds of marine origin are not biotransformed to inorganic arsenic or methylated arsenic acids to any significance in the human body. They do not produce arsines when treated with the reducing agent in the proposed method and will therefore not interfere with the measurements. The sensitivity, accuracy, and precision of the proposed method are sufficient for the determination of concentrations of arsenic normally found in the urine of nonexposed persons. The method is based on a commercially available hydride generation kit attached to an atomic absorption spectrophotometer.

Arsenic↗
PubMedDate not supplied

Arsenic trioxide in the management of acute promyelocytic leukaemia.

Arsenical compounds were used as early as 2000 BC, both as medicines as well as poisons. Arsenicals gained importance in the beginning of the last century as the primary mode of treating syphilis. In 1931, Folkner and Scott used an arsenical preparation called Fowler's solution in the treatment of chronic myeloid leukaemia. This continued to be used until the introduction of busulphan in 1953. In the 1970s, arsenic trioxide was introduced for the treatment of acute promyelocytic leukaemia in China and was found to be extremely effective in treating this condition. Since then, numerous in vitro and in vivo studies have confirmed this observation. This article reviews the pathogenesis of acute promyelocytic leukaemia, the possible mechanism of action of arsenic trioxide in this condition and the literature on its use in the treatment, with special reference to the clinical and molecular response rates, toxicity and pharmacology of this compound. It also attempts to address the role of arsenic trioxide in the present algorithm for the treatment of acute promyelocytic leukaemia.

Adolescent↗
PubMed2002

Microbial arsenic: from geocycles to genes and enzymes.

Arsenic compounds have been abundant at near toxic levels in the environment since the origin of life. In response, microbes have evolved mechanisms for arsenic resistance and enzymes that oxidize As(III) to As(V) or reduce As(V) to As(III). Formation and degradation of organoarsenicals, for example methylarsenic compounds, occur. There is a global arsenic geocycle, where microbial metabolism and mobilization (or immobilization) are important processes. Recent progress in studies of the ars operon (conferring resistance to As(III) and As(V)) in many bacterial types (and related systems in Archaea and yeast) and new understanding of arsenite oxidation and arsenate reduction by respiratory-chain-linked enzyme complexes has been substantial. The DNA sequencing and protein crystal structures have established the convergent evolution of three classes of arsenate reductases (that is classes of arsenate reductases are not of common evolutionary origin). Proposed reaction mechanisms in each case involve three cysteine thiols and S-As bond intermediates, so convergent evolution to similar mechanisms has taken place.

Arsenate Reductases↗
PubMed2006

Arsenic derivatives in hematologic malignancies: a role beyond acute promyelocytic leukemia?

The importance of arsenic trioxide (As2O3) has been underscored over the last decade due to its efficacy against acute promyelocytic leukemia (APL), a disease in which this agent has been associated with complete hematologic and molecular remission rates of 87% and 83%, respectively. The different molecular mechanisms of action of As2O3 suggest its applicability in hematologic malignancies other than APL. However, responses obtained thus far have consisted of improvements in signs and symptoms without the elimination of a given disease. Toxicities derived from As2O3 are significant but manageable and reversible. However, the risk/benefit ratio of As2O3 in hematologic malignancies other than APL is still unclear. The development of new generations of orally bioavailable inorganic, as well as new organic, arsenic compounds with improved toxicity profiles may bolster the therapeutic application of arsenic derivatives in hematologic malignancies such as leukemia, multiple myeloma and myelodysplastic syndromes.

Administration, Oral↗
PubMed2002

Monitoring of arsenic exposure with speciated urinary inorganic arsenic metabolites for ion implanter maintenance engineers.

For wafer fabrication in the semiconductor industry, maintenance engineers are potentially exposed to hazards during their work of disassembling machine components for cleanup. One special concern is the presence of arsenic or arsenic compounds in the working environment. This study analyzed speciated urinary inorganic arsenic metabolites of the maintenance engineers using high-performance liquid chromatography-hydride generation atomic absorption spectrometry to study the potential arsenic exposure during their maintenance work. In total, from six wafer fabrication facilities, 30 maintenance engineers were recruited as the exposed group and another 12 office-based engineers served as the control group. First morning-voided urine samples of each study subject were collected for 7 consecutive days. The levels of total urinary inorganic arsenic metabolites for the exposed group were 1.7+/-1.4, 1.4+/-1.1, 6.2+/-6.7, 20.2+/-14.1, and 29.5+/-17.2 micro g/L for As3+, As5+, monomethylarsonic acid, dimethylarsinic acid, and total inorganic arsenic, respectively. Both the concentration of monomethylarsonic acid and its percentage in total urinary inorganic arsenic metabolites showed significantly ascending trends for the control group, for the engineers without preventative maintenance work prior to their urine sampling, and for the engineers with such work prior to their urine sampling (P<0.05 and P<0.0005, respectively). The data also suggested that, at low-level occupational arsenic exposure, the concentration of total urinary inorganic arsenic metabolites might be misleading due to the confounding effect resulting from intake of seafood, such as arsenosuger. Nevertheless, monitoring of urinary arsenic species by using the percentage change of monomethylarsonic acid in total urinary inorganic arsenic metabolites as an indicator for the verification of arsenic exposure is helpful and appropriate in such cases.

Adult↗
PubMed2001

Arsenic extraction and speciation in carrots using accelerated solvent extraction, liquid chromatography and plasma mass spectrometry.

Arsenic present in freeze-dried carrots was extracted using accelerated solvent extraction (ASE). Several parameters, including selection of the dispersing agent, extraction time, number of extraction cycles, particle size and extraction temperature, were evaluated to optimize the ASE method. Filtering and treatment with C-18 SPE cartridges were also evaluated as part of the sample preparation procedure before speciation analysis. The method was validated by spiking single arsenical and mixed arsenical standards on the dispersing agent and on portions of freeze-dried carrot prior to extraction. LC-ICP-MS was used to determine individual arsenic species in the carrot extracts. A weak anion-exchange column was used for the separation of As(III), As(v), monomethylarsonic acid (MMA), dimethylarsinic acid and arsenobetaine. Optimized sample preparation conditions were applied to the extraction of arsenic in nine freeze-dried carrot samples. Total arsenic concentration in the carrot samples ranged from less than 20 ng g(-1) to 18.7 microg g(-1), dry mass. Extraction efficiency, defined as the ratio of the sum of individual arsenic species concentrations to total arsenic, ranged from 80 to 102% for freeze-dried carrots with arsenic concentrations greater than the limit of quantitation. Inorganic As(III) and As(v) were the only species found in samples that contained less than 400 ng g(-1) total arsenic. MMA and an unidentified arsenic compound were present in some of the samples with higher total arsenic content.

Arsenic↗
PubMed2006

Arsenic and cigarette smoke synergistically increase DNA oxidation in the lung.

Epidemiological evidence has indicated that arsenic and cigarette smoking exposure act synergistically to increase the incidence of lung cancer. Since oxidative damage of DNA has been linked to cancer, our hypothesis is that aerosolized arsenic and cigarette smoke work synergistically to increase oxidative stress and increase DNA oxidation in the lung. To test this hypothesis male Syrian golden hamsters were exposed to room air (control), aerosolized arsenic compounds (3.2 mg/m3 for 30 minutes), cigarette smoke (5 mg/m3 for 30 minutes), or both smoke and arsenic. Exposures were for 5 days/week for 5 or 28-days. Animals were sacrificed one day after the last exposure. In the 28-day group, glutathione levels and DNA oxidation (8-oxo-2'-deoxyguanosine (8-oxo-dG)) were determined. Our results show that in the 28-day arsenic/smoke group there was a significant decrease in both the reduced and total glutathione levels compared with arsenic or smoke alone. This correlated with a 5-fold increase in DNA oxidation as shown by HPLC. Immunohistochemical localization of 8-oxo-dG showed increase staining in nuclei of airway epithelium and subadjacent interstitial cells. These results show that dual exposure of arsenic and cigarette smoke at environmentally relevant levels can act synergistically to cause DNA damage.

8-Hydroxy-2'-Deoxyguanosine↗