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Glycidyl fatty acid esters (GE) are constituents of edible oils and fats, and are converted into glycidol, a genotoxic substance, in vivo.  N -(2,3-dihydroxypropyl)valine (diHOPrVal), a hemoglobin adduct of glycidol, is used as a biomarker of glycidol and GE exposure. However, high background levels of diHOPrVal are not explained by daily dietary exposure to glycidol and GE. In the present study, several glycidol-related chemicals (glycidol, (±)-3-chloro-1,2-propanediol, glycidyl oleate, epichlorohydrin, propylene oxide, 1-bromopropane, allyl alcohol, fructose, and glyceraldehyde) that might be precursors of diHOPrVal, were administered to mice, and diHOPrVal formation from each substance was examined with LC-MS/MS. DiHOPrVal was detected in animals treated with glycidol and glycidyl oleate but not in mice treated with other chemicals (3-MCPD, epichlorohydrin, propylene oxide, 1-bromopropane, allyl alcohol, fructose, and glyceraldehyde). The amount of diHOPrVal per administered dose produced from other chemicals was negligible compared to the amounts associated with dietary glycidol and GE. The present study provides important knowledge for exploring other sources for internal exposure to glycidol.

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Does External Exposure of Glycidol-Related Chemicals Influence the Forming of the Hemoglobin Adduct, N-(2,3-dihydroxypropyl)valine, as a Biomarker of Internal Exposure to Glycidol?