Browsing by Subject "arsenate"
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Item Adsorption of As(V), As(III) and methyl arsenic by calcite and the impact of some groundwater species(2009-05-15) Jones, Robert GarretThe objective of this research was to investigate the retention of arsenate (iAsV), arsenite (iAsIII), monomethyl arsenate (MMAsV) and dimethyl arsenate (DMAsV) by calcite and assess the impact of dissolved Ca2+, Mg2+, phosphate and sulfate on arsenic solubility, adsorption and precipitation phenomena. Adsorption kinetics of iAsV, evaluated at a low and high concentration, was a relatively rapid process, with a fast initial reaction rate within the first few minutes and a subsequent slower reaction rate as equilibrium was approached. The relative adsorption of arsenicals decreased in the following order: iAsV > iAsIII > DMAV > MMAV. In no case was a clear adsorption maximum observed with increasing dissolved arsenic concentration. Dissolved 0.01 M Ca2+ resulted in an increase in iAsV adsorption; however, in the presence of 0.1 M Ca2+ adsorption of iAsV was decreased. The presence of Mg2+ as 0.01 M Mg(NO3)2 resulted in decreased iAsV adsorption probably the result of a lower iAsV affinity for adsorbed Mg2+ as compared to Ca2+. Phosphate and sulfate were highly competitive with iAsV in adsorption to calcite and both resulted in decreased iAsV adsorption. The total prevention of iAsV adsorption at initial equimolar arsenic/phosphate concentrations > 88 ?M each could be from the consumption of available calcite surface sites by the specific adsorption of phosphate. Equilibrium modeling, using the geochemical and mineral speciation of equilibrium model (MINTEQA2), indicated that at low concentrations of arsenate or phosphate solid-phase precipitation was not likely and adsorption processes likely controlled solubility. At high concentrations of arsenate Ca3(AsO4)2 ? 3 2/3 H2O and Ca3(AsO4)2 ? 4 1/4 H2O solid phases could be controlling arsenate solubility. This study indicates that arsenic adsorption response by calcite was different than that of phosphate suggesting that arsenic may not be specifically adsorbed to calcium at the calcite surface. Reduction and biomethylation of arsenic decreased adsorption, suggesting that processes which could affect the speciation of arsenic in the environment, could increase arsenic mobility in environmental systems where calcite and dissolved aqueous calcium play a predominant role in controlling arsenic solubility. Dissolved aqueous concentrations of magnesium, phosphate and sulfate generally reduced the ability of arsenic to be adsorbed to calcite.Item Investigations into arsenate-induced neural tube defects in a mouse model(2009-05-15) Hill, Denise SuzanneNeural tube defects (NTDs) are malformations affecting about 2.6/1000 births worldwide, and 1/1000 in the United States. Their etiology remains unknown, and is likely due to interaction of genetic susceptibility factors with environmental exposure. Of the many environmental agents considered to potentially contribute to NTD risk, arsenic is one that is surrounded in controversy. We have developed a model system utilizing maternal intraperitoneal (I.P.) exposure on E7.5 and E8.5 to As 9.6 mg/kg (as sodium arsenate) in a normal inbred mouse strain, LM/Bc/Fnn, that is sensitive to arsenate-induced exencephaly. We investigated arsenate induced gene expression changes using DNA microarrays of embryonic anterior neural tube tissue, as well as monitoring of metabolic function in conjunction with the administration of select compounds to rescue the normal phenotype. Finally, to address questions concerning the importance of route of administration and potential maternal toxicity, a teratology study was performed using three arsenate doses administered orally. Regarding the gene expression study, we identified several candidate genes and ontology groups that may be responsible for arsenate?s teratogenicity. Genes include: engrailed 1 (En-1), platelet derived growth factor receptor alpha (Pdgfr?) and ephrinA7 (EphA7). Gene ontology groups identified include oxidative phosphorylation, redox response, and regulation of I-kappaB kinase/NF-kappaB cascade. Acute arsenate exposure induced disruption of mitochondrial function and dependent glucose homeostasis: subsequent hyperglycemia was teratogenic. Maternal treatment with insulin or n-acetyl cysteine, an antioxidant and precursor of glutathione synthesis, proved highly successful in rescuing both the normal phenotype, and to differing degree, the maternal hyperglycemia. Maternal oral arsenate administration also resulted in exencephaly, with exposed embryos exhibiting a positive linear trend with arsenate dosage. There were also linear trends in the relationships between arsenate dose and anomalies involving several components of the axial skeleton: the vertebrae and calvarium. There was no evidence of maternal toxicity as shown by lack of differences in maternal body weight gain, liver, and kidney weights. In conclusion, maternal arsenate exposure (regardless of exposure route) was teratogenic in our model, primarily causing NTDs. Responsible mechanisms may involve disruption of redox and glucose homeostasis as well as expression of established NTD candidate genes.