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    Determination of endogenous and exogenously derived N7-(2-hydroxyethyl)guanine adducts in ethylene oxide-treated rats.

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    Authors
    Marsden, Debbie A.
    Jones, Donald J.L.
    Lamb, John H.
    Tompkins, Elaine M.
    Farmer, Peter B.
    Brown, Karen
    Issue Date
    2007-02
    
    Metadata
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    Abstract
    Ethylene oxide (EO) is one of the most widely used intermediates in the chemical industry. It is also formed endogenously as a result of cytochrome P450-mediated metabolism of ethylene, which is ubiquitous in the environment. Additionally, ethylene is generated in vivo during normal physiological processes such as methionine oxidation and lipid peroxidation; therefore, humans are continually exposed to EO. EO is classed by the IARC as carcinogenic to humans and reacts with DNA, primarily forming N7-(2-hydroxyethyl)guanine adducts (N7-HEG), which can be used as biomarkers of exposure and potential cancer risk. To assess the risks to humans associated with occupational exposure to low EO concentrations, it is necessary to establish the relative contribution of DNA damage arising from endogenous and exogenously derived EO. Using a newly developed highly sensitive LC-MS/MS assay with selected reaction monitoring that offers a limit of detection of 0.1 fmol of N7-HEG on column, we have established background levels of N7-HEG (1.1-3.5 adducts/10(8) nucleotides) in tissues of rats. Following intraperitoneal administration of a single dose or three daily doses of EO (0.01-1.0 mg/kg), N7-HEG adducts generally increased with dose, except at the lowest concentration where total N7-HEG levels were no different to that detected in control animals, indicating that any increase was negligible as compared to the endogenous damage already present. In the 3 day study, the kinetics of adduct removal were also investigated and in comparing N7-HEG formation in the two studies, DNA damage did not appear to accumulate with repeated administration.
    Citation
    Chem. Res. Toxicol. 2007, 20 (2):290-299
    Journal
    Chemical Research in Toxicology
    URI
    http://hdl.handle.net/10146/25472
    DOI
    10.1021/tx600264t
    PubMed ID
    17263564
    Additional Links
    http://pubs.acs.org/cgi-bin/abstract.cgi/crtoec/2007/20/i02/abs/tx600264t.html
    Type
    Article
    Language
    en
    ISSN
    0893-228X
    ae974a485f413a2113503eed53cd6c53
    10.1021/tx600264t
    Scopus Count
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