Elucidating pathway arsenic methylation


15-Jul-2015 08:58

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Genetic predisposition of individuals affects disease outcome. E-mail: [email protected] apologize to our colleagues whose quality work may not have been cited because of word count limitations.Interactions with infectious agents, particularly viruses, may explain some species-specific differences between human pathologies and experimental animal pathologies. We acknowledge support from the National Institutes of Health (grants R21ES015812, R21ES015812-02S2, P30ES014443, R21ES017235, P30ES006096, P42ES004940, P30ES006694, R01ES010807, R01ES013781, and R01ES013781-02S1) and the U. Environmental Protection Agency (grant R832095-010). This article is based in part on discussions held during the “Workshop on Phenotypic Anchoring of Arsenic Dose/Exposure in Experimental Models of Human Disease,” held at the University of Louisville, Louisville, Kentucky, 21 October 2010.We propose phenotypic anchoring as a means to unify experimental observations and disease outcomes.Objectives: We examined the use of phenotypic anchors to translate experimental data to human pathology and investigated research needs for which phenotypic anchors need to be developed.Conclusions: Translation to human populations requires more extensive profiling of human samples along with high-quality dosimetry.Anchoring results by gene expression and epigenetic profiling has great promise for data unification.

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In a literature review, we identified areas where data exist to support phenotypic anchoring of experimental results to pathologies from specific human exposures.Translation of laboratory arsenic toxicology studies to human health is important but is complicated by inexact dose conversion between , murine, and human exposures and species-specific metabolic differences.Discussion: Disease outcome is likely dependent on cell-type–specific responses and interaction with individual genetics, other toxicants, and infectious agents.Potential phenotypic anchors include target tissue dosimetry, gene expression and epigenetic profiles, and tissue biomarkers.

Background: Chronic arsenic exposure is a worldwide health problem.

How arsenic exposure promotes a variety of diseases is poorly understood, and specific relationships between experimental and human exposures are not established.



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