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Chronic Arsenic Exposure and Blood Glutathione and Glutathione Disulfide Concentrations in Bangladeshi Adults
Author(s) -
Megan N. Hall,
Megan M. Niedzwiecki,
Xinhua Liu,
Kristin N. Harper,
Shafiul Alam,
Vesna Slavkovich,
Vesna Ilievski,
David E. Levy,
Abu Baker Siddique,
Faruque Parvez,
Jacob L. Mey,
Alexander van Geen,
Joseph H. Graziano,
Mary V. Gamble
Publication year - 2013
Publication title -
environmental health perspectives
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.257
H-Index - 282
eISSN - 1552-9924
pISSN - 0091-6765
DOI - 10.1289/ehp.1205727
Subject(s) - glutathione , arsenic , arsenic toxicity , glutathione disulfide , chemistry , environmental chemistry , physiology , medicine , toxicology , biochemistry , biology , enzyme , organic chemistry
In vitro and rodent studies have shown that arsenic (As) exposure can deplete glutathione (GSH) and induce oxidative stress. GSH is the primary intracellular antioxidant; it donates an electron to reactive oxygen species, thus producing glutathione disulfide (GSSG). Cysteine (Cys) and cystine (CySS) are the predominant thiol/disulfide redox couple found in human plasma. Arsenic, GSH, and Cys are linked in several ways: a) GSH is synthesized via the transsulfuration pathway, and Cys is the rate-limiting substrate; b) intermediates of the methionine cycle regulate both the transsulfuration pathway and As methylation; c) GSH serves as the electron donor for reduction of arsenate to arsenite; and d) As has a high affinity for sulfhydryl groups and therefore binds to GSH and Cys.

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