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    Elucidating pathway arsenic methylation

    A two-stage regression analysis approach was followed.First, generalized linear models were used to assess the relation between each of the five dietary As measures and u As LOD, and general linear and mixed models were run using bootstrap sampling with replacement (500 replications) from the entire population. Waters is handling the molecular biology for the Molecular and Physiological Imaging Lab. (1997) Factors affecting 5-methylcytosine-to- thymine transitions in the p53 gene of colorectal cancers.Mostly he is cloning and measuring gene expression using real-time PCR. (Biology), Davidson College, Davidson, North Carolina, May 1993 Ph. (Molecular Genetics), Wake Forest University School of Medicine, Winston-Salem, North Carolina, December 2001 Thesis: Investigations on the repair of G: U and G: T mispairs arising from the spontaneous deamination of cytosine and 5-methylcytosine. Li J, Waters SB, Drobn Z, Devesa V, Styblo M, Thomas DJ. Hart LS, Yannone SM, Naczki C, Orlando J, Waters SB, Akman SA, Chen DJ, Ornelles D, Koumenis C. Waters SB, Devesa V, Fricke MW, Creed JT, Styblo M, Thomas DJ. Drobn Z*, Waters SB*, Walton FS, Le Cluyse EL, Thomas DJ, Stblo M. * Authors contributed equally to the research presented in this manuscript Devesa V, Del Razo LM, Adair B, Drobn Z, Waters SB, Hughes MF, Styblo M, Thomas DJ. Waters SB, Devesa V, Del Razo, Styblo M, and Thomas DJ. Walton FS, Waters SB, Jolley SL, Le Cluyse EL, Thomas DJ, Styblo M. Styblo M., Waters SB, Drobn Z, Lin S, Walton FS, Jaspers I, Patel YM, Del Razo LM, Thomas D. (2003) Production and biological significance of methylated trivalent arsenicals. Proceedings of International Symposium on Bio-Trace Elements 2002, 10/28-11/2, Tokyo, Japan, pp. Waters SB, Walker L, Farman GP, de Tombe P and Buttrick PM(2005) TAT-mediated Transduction Of Structural and Regulatory Myofilament Proteins. NATO Advanced Study Institute, Advances in DNA Damage and Repair.Society of Toxicology Annual meeting, Baltimore, Maryland Waters SB, Styblo M, Beck MA, Thomas DJ (2002) Cloning, expression and mutational analysis of the rat S-adenosyl-L-methionine:arsenic(III) methyltransferase. Exposure to inorganic arsenic (i As) from water, food, and ambient air is widespread (Franklin et al. In addition, the present study was specifically approved by the SHS Publications and Presentations Committee and by the participating tribes. Spot urine samples were collected in 1989–1991, frozen within 1–2 hr of collection, and stored at –80ºC at the Penn Medical Laboratory, Med Star Health Research Institute (Hyattsville, MD, and Washington, DC, USA) (Lee et al. In 2009, up to 1.0 m L of urine from each participant was transported on dry ice to the Trace Element Laboratory of the Institute of Chemistry–Analytical Chemistry, Karl-Franzens University (Graz, Austria). Genetic variations associated with interindividual sensitivity in the response to arsenic exposure. Hernandez A, Xamena N, Sekaran C, Tokunaga H, Sampayo-Reyes A, Quinteros D, et al. High arsenic metabolic efficiency in AS3MT287Thr allele carriers. Hopenhayn-Rich C, Biggs ML, Kalman DA, Moore LE, Smith AH. Arsenic methylation patterns before and after changing from high to lower concentrations of arsenic in drinking water. Hopenhayn-Rich C, Biggs ML, Smith AH, Kalman DA, Moore LE. Methylation study of a population environmentally exposed to arsenic in drinking water. Polymorphisms in arsenic (III) methyltransferase () have been consistently associated with urine arsenic methylation patterns in populations from Argentina (Schlawicke et al. Participants were similar to nonparticipants in age, body mass index (BMI), and self-reported frequency of diabetes. Starting in 1998, the Strong Heart Family Study (SHFS) recruited persons who were ≥ 18 years of age and extended family members of the original SHS participants to participate in a study of the genes that contribute to cardiometabolic risk in American Indian populations (North et al. For the SHFS, families who had at least five living siblings, including three original SHS participants, were invited; and parents, spouses, offspring, spouses of offspring, and grandchildren were enrolled to build extended pedigrees. : The Environmental Protection Agency calls arsenic the most prevalent environmental toxin and carcinogen in the United States (://

    Individuals with AS3MT polymorphisms produce increased amounts of methylated species.Modeling of urinary total arsenic was completed in the ABS, NHEXAS-AZ and the two populations combined.Due to a high proportion of u As values below the limit of detection (LOD) of 4.7 µg/L, u As exposure was evaluated as a binary variable, above or below the LOD, and, for values above the LOD, as a continuous, log-transformed variable. Humans metabolize i As (arsenate and arsenite) to methylated compounds [predominantly monomethylarsonate (MMA) and dimethylarsinate (DMA)], which are largely excreted in urine together with i As (Cullen and Reimer 1989; Naranmandura et al. In human populations, the average distribution of arsenic metabolites in urine is approximately 10–30% i As, approximately 10–20% MMA, and approximately 60–80% DMA (Chiou et al. The present heritability and linkage study was covered by the original SHS consent form because arsenic is a potential cardiovascular risk factor. All participants provided written and oral informed consent at enrollment into the SHS. Environmental chemical exposures and human epigenetics.

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