Intake of Inorganic Arsenic in the North American Diet

Dietary intake of inorganic arsenic, previously assumed to be an insignificant source of arsenic exposure in humans, was estimated for Canadian and United States populations. Input data included arsenic contents of various food groups, a limited historical database from the Ontario Ministry of the Environment measuring the percent inorganic arsenic in food groups, and food consumption data. Estimated daily dietary intake of inorganic arsenic ranges from 8.3 to 14?µg/day in the United States and from 4.8 to 12.7?µg/day in Canada for various age groups. These data suggest that between 21% to 40% of total dietary arsenic occurs in inorganic forms. Uncertainties regarding total arsenic in dairy products in the data set applied here may account for observed differences between United States and Canadian estimates. While estimates provided here are preliminary because of limitations in data on the proportion of inorganic arsenic in foods, this analysis suggests that dietary intake of inorganic arsenic is higher than is currently assumed. Additional research is needed to more fully characterize inorganic arsenic concentrations in foods. Future study is also needed on the variability of total and inorganic arsenic in foods and the bioavailability of dietary inorganic arsenic.     

Study on the effects of arsenic pollution on the communities of macro-invertebrate in Xieshui River

In 2006 and 2007, five sampling stations were set up in Xieshui River and its tributaries to study the macro-invertebrate communities, and measure physicochemical parameters and contents of different forms of arsenic. A comparative analysis and multivariate statistical methods were used to explore the effects of arsenic pollution on the macro-invertebrate communities. In this study, sixty species were identified, including 39 aquatic insects, 10 mollusks, 5 oligochaetes, 1 crustacean, and 5 others. Results of the comparative analysis indicated that the macro-invertebrate communities at the station with serious arsenic pollution tended to be simple and showed a significant decreasing in density, biomass, and biodiversity in comparison with the other stations. Arsenic pollution also had a major effect on the dominant species and groups. For instance, EPT taxa disappeared at the station with serious arsenic pollution, and chironomids that belong to the genus Cardiocladius were very tolerant to high concentrations of arsenic. Results of the functional feeding groups (FFGs) analysis indicated that the predators were more tolerant to arsenic pollution, while the scrapers, filterers, and collectors were relatively sensitive to arsenic pollution. Results of a non-metric multidimensional scaling (nMDS) analysis showed that when the concentration of inorganic arsenic decreased to the range between the criteria continuous concentration (CCC) and the criteria maximum concentration (CMC), the effects of inorganic arsenic on the macro-invertebrate communities seemed to be insignificant. Results of a BVSTEP (Bio-Env Step-Wise Procedure) analysis showed that water temperature, rotifer density, trivalent arsenic, pentavalent arsenic, and total inorganic arsenic greatly influenced species appearance, while rotifer density and various forms of arsenic had a considerable impact on the species composition.     

Comparative Molecular Docking Studies with ABCC1 and Aquaporin 9 in the Arsenite Complex Efflux

Arsenic is the most toxic metalloid present in the natural environment in both organic and inorganic arsenic forms. Inorganic arsenic is often more hazardous than the organic form. Arsenite and arsenate compounds are the major inorganic forms which are toxic causing severe human health dysfunction including cancer. Excretion of arsenic from the system is found elusive. Therefore, it is of interest to screen channel proteins with the arsenic complex in the different combination of arsenic, GSH (glutathione) and arsenic, selenium using docking methods. The mode of arsenic removal. The complex structure revealed the mode of arsenic binding efficiency with the receptor aquaporine 9 and ABCC1 channel protein. This provides insights to understand the mechanism of arsenic efflux. These inferences find application in the design, identification and development of novel nutracetucal or any other formulation useful in the balance of arsenic efflux.     

Importance of Arsenic Speciation in Populations Exposed to Arsenic in Drinking Water

Total arsenic in urine is often the principal means for assessing chronic exposure to arsenic-contaminated drinking water. This approach ignores many components of the human diet, especially fish and seafood that contain arsenic at significant concentrations. The toxicity differences between the inorganic forms and the dietary forms suggest both should be evaluated when attempting to assess risk from arsenic exposure. Urine biomonitoring for 53 participants was used to confirm reduction in arsenic exposure resulting from well water remediation removing inorganic arsenic from drinking water. Initially, only total arsenic urine assays were performed, but spikes in total arsenic urine concentrations were determined to be diet related and demonstrated the need for analytical methods that differentiate the arsenic species. A secondary analysis was added that quantified inorganic-related arsenic in urine and the dietary forms related to fish and seafood by subtraction from total arsenic. Significant differences were found between the inorganic arsenic component and the total arsenic measured in their urine. On average, approximately 76% of total arsenic in urine was attributed to fish and other organo-arsenic dietary sources, implying a potential significant overestimate of exposure, and demonstrating the need for differentiation of the inorganic-related arsenic from dietary arsenic.     

Arsenic and cadmium in the marine macroalgae (Porphyra yezoensis and Laminaria Japonica) — forms and concentrations

Abstract

Total arsenic, inorganic arsenic (iAs), total cadmium concentrations and chemical forms of cadmium were analysed in Porphyra yezoensis collected monthly from January to April in 2011 and in Laminaria Japonica collected monthly from March to July in 2010. Results showed that total As concentrations in P. yezoensis were much lower than those in L. Japonica. The iAs concentrations in both macroalgae were all below the maximum limit according to the legislation in China, while total Cd concentrations in all samples of P. yezoensis exceeded the maximum limit. The percentage of iAs to total As decreased in both macroalgae with the time. The results provide important information showing that both macroalgae are able to metabolise inorganic arsenic to organic forms. Thus both macroalgae have evolved arsenic resistance which is linked to the capability of metabolising toxic inorganic arsenic. In addition, the results suggest that the transformation rate of arsenate to organic arsenic in both algae increases with the growth and metabolic rate that increase with elevated environmental temperature. Temperatures rise from January to April in Jiangsu province and from March to July in Liaoning Province. Most Cd was associated with pectates and protein (extractable by 1 M NaCl) in both algae, and only a small percentage of the Cd was inorganic (extractable by 80% ethanol). The Cd chemical forms have no obvious relationship with the time in both algae.     

Biological Responses to Arsenic Compounds

Arsenic is a metalloid that generates various biological effects on cells and tissues. Depending on the specific tissue exposed and the time and degree of exposure, diverse responses can be observed. In humans, prolonged and/or high dose exposure to arsenic can have a variety of outcomes, including the development of malignancies, severe gastrointestinal toxicities, diabetes, cardiac arrhythmias, and death. On the other hand, one arsenic derivative, arsenic trioxide (As₂O₃), has important antitumor properties. This agent is a potent inducer of antileukemic responses, and it is now approved by the Food and Drug Administration for the treatment of acute promyelocytic leukemia in humans. The promise and therapeutic potential of arsenic and its various derivatives have been exploited for hundreds of years. Remarkably, research focused on the potential use of arsenic compounds in the treatment of human diseases remains highly promising, and it is an area of active investigation. An emerging approach of interest and therapeutic potential involves efforts to target and block cellular pathways activated in a negative feedback manner during treatment of cells with As₂O₃. Such an approach may ultimately provide the means to selectively enhance the suppressive effects of this agent on malignant cells and render normally resistant tumors sensitive to its antineoplastic properties.Arsenic forms complexes with other elements, and it exists in inorganic and organic forms (1–3). The three major inorganic forms of arsenic are arsenic trisulfide (As₂S₃, yellow arsenic), arsenic disulfide (As₂S₂, red arsenic), and arsenic trioxide (As₂O₃, white arsenic) (1–3). There are two different oxidative states of arsenic that correlate with its cytotoxic potential, As(III) and As(V). Among them, As(III) is the most potent form and primarily accounts for its pro-apoptotic and inhibitory effects on target cells and tissues (3). The various forms of arsenic exist in nature primarily in a complex with pyrite (4, 5), although under certain circumstances, arsenic can dissociate from soil and enter natural waters (6), providing a contamination source for humans or animals who ingest such waters. In fact, most associations between long term exposure to arsenic and development of malignancies or other health disorders result from drinking contaminated water, especially in developing countries. Interestingly, pollution of the air with arsenic can also occur under certain circumstances, such as in the case of emissions from coal burning in China (7), providing an additional source of human exposure.The metabolism of arsenic in humans includes reduction to the trivalent state and oxidative methylation to the pentavalent state (reviewed in Ref. 2). There is also reduction of arsenic acid to the arsenous form and subsequent methylation (2). The generation of inorganic or organic trivalent arsenic forms has important implications with regard to the toxicity of this agent, as such compounds are more toxic to the cells and exhibit more carcinogenic properties (2, 3). Thus, many of the consequences of exposure to arsenic as discussed below are the result of the activities and toxicities of the various metabolic products of arsenic compounds. It should be also noted that arsenic has the ability to bind to reduced thiols, including sulfhydryl groups in some proteins (2). Depending on the cellular context, such protein targeting may explain some of its cellular effects and generation of its toxicities and/or therapeutic effects.     

Arsenic (+3 oxidation state) methyltransferase and the methylation of arsenicals

Metabolic conversion of inorganic arsenic into methylated products is a multistep process that yields mono-, di-, and trimethylated arsenicals. In recent years, it has become apparent that formation of methylated metabolites of inorganic arsenic is not necessarily a detoxification process. Intermediates and products formed in this pathway may be more reactive and toxic than inorganic arsenic. Like all metabolic pathways, understanding the pathway for arsenic methylation involves identification of each individual step in the process and the characterization of the molecules which participate in each step. Among several arsenic methyltransferases that have been identified, arsenic (+3 oxidation state) methyltransferase is the one best characterized at the genetic and functional levels. This review focuses on phylogenetic relationships in the deuterostomal lineage for this enzyme and on the relation between genotype for arsenic (+3 oxidation state) methyltransferase and phenotype for conversion of inorganic arsenic to methylated metabolites. Two conceptual models for function of arsenic (+3 oxidation state) methyltransferase which posit different roles for cellular reductants in the conversion of inorganic arsenic to methylated metabolites are compared. Although each model accurately represents some aspects of enzyme's role in the pathway for arsenic methylation, neither model is a fully satisfactory representation of all the steps in this metabolic pathway. Additional information on the structure and function of the enzyme will be needed to develop a more comprehensive model for this pathway.