Volume 89 Issue 8 | pp. 33-34 | Concentrates
Issue Date: February 21, 2011

Epigenetic Clues To Arsenic Toxicity

Newly identified tumor-suppressor genes could help unravel how long-term arsenic exposure leads to diseases
Department: Science & Technology
News Channels: Environmental SCENE
Keywords: arsenic, epigenetics, DNA methylation, toxicity

Long-term exposure to low levels of arsenic in drinking water—a public health problem affecting tens of millions of people globally—is associated with an increased incidence of heart disease, diabetes, and cancer. Studies on arsenic poisoning have identified epigenetic changes such as altered DNA methylation as a probable cause of these health effects, but it’s still unclear whether multiple genes and pathways are affected. Toxicologists led by Rebecca C. Fry of the University of North Carolina, Chapel Hill, now report the first study to examine genomewide, site-specific DNA methylation in people with ongoing exposure to arsenic (Chem. Res. Toxicol., DOI: 10.1021/tx1004419). The researchers mapped the “methylome,” or differentially methylated genomic regions, associated with arsenic exposure in people from Zimapán, Mexico, a town with arsenic-tainted water stemming from mining operations. Using a series of assays, the team examined 14,000 genes isolated from blood lymphocyte DNA and found 183 genes with altered methylation patterns. The researchers also uncovered 17 tumor-suppressor genes known to be silenced by arsenic toxicity and kept from fulfilling their role to protect cells from cancer. This “suppressorome” significantly increases the list of gene targets and “represents a pivotal clue in unraveling a possible epigenetic mode of arsenic-induced disease,” Fry and coworkers write.

 
Chemical & Engineering News
ISSN 0009-2347
Copyright © American Chemical Society

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