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Research: Bruce Stanton's scientific interests include the cellular and molecular mechanisms underlying genetic diseases and how environmental toxins, including arsenic, affect disease progression and outcome. The objective of one of his studies is to elucidate how arsenic, a toxic metalloid, affects xenobiotic bioavailability and increases the incidence of atherosclerotic disease, diabetes mellitus as well as several types of drug resistant cancers. In particular his research is focused on elucidating the effects of low, environmentally relevant levels of arsenic on the expression and function of two ABC (ATP Binding Cassette) transporters: the cystic fibrosis transmembrane conductance regulator (CFTR) and the multidrug resistance protein 2 (MRP2). CFTR is a cAMP-activated Cl channel, and plays an important role in salt homeostasis. MRP2 transports xenobiotics, including chemotherapeutic drugs, toxins, and arsenic-glutathione conjugates out of cells and, thereby, plays a role in xenobiotic excretion in bile and urine, protects the brain from xenobiotic and toxic compounds and limits the intestinal absorption of drugs. His laboratory has shown that environmentally relevant levels of arsenic blocks the ability of CFTR to regulate salt balance in the teleost Fundulus heteroclitus. By contrast, they have found that arsenic increases the functional expression of MRP2 in kidney and colon, and thereby increases xenobiotic excretion and limits xenobiotic bioavailability. Dr. Stanton’s laboratory examines the effects of arsenic in two model systems: the euryhaline teleost Fundulus heteroclitus, and polarized human colonic Caco-2 epithelial cells.