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comments: Should parent compound not be acrylamide? INCHIKEY Does not seem to correspond to the correct compound Pubchem link to AAVal: https://pubchem.ncbi.nlm.nih.gov/substance/341427830 vs Pubchem link to related compound with INCHI key specified here: https://pubchem.ncbi.nlm.nih.gov/compound/N-_3-Amino-3-oxopropyl_-L-valine --> chemical structure is not the same so I don't know if these are the same compounds? feedback_epi team: Yes assigning Acrylamide as parent compound seems correct to me. Because Acrylamide is the substance a human is exposed to, and we can measure GAVAL and AAVAL to reflect that exposure. GA‑Val (GAVAL) and AA‑Val (AAVAL) — are both well‑established biomarkers of exposure to acrylamide and its metabolite glycidamide. These adducts form when the reactive compounds bind to the N‑terminal valine of hemoglobin. Core attribution - AAVAL (N‑(2‑carbamoylethyl)valine) reflects exposure to acrylamide, the parent compound. - GAVAL (N‑(2‑carbamoyl‑2‑hydroxyethyl)valine) reflects exposure to glycidamide, which is the epoxide metabolite formed when acrylamide is metabolized via CYP2E1. This relationship is well documented: acrylamide is converted to glycidamide, and both acrylamide and glycidamide form hemoglobin adducts that can be used to reconstruct exposure. source: https://pmc.ncbi.nlm.nih.gov/articles/PMC5696489/ Moreover, AA and GA react with plasma and other proteins, such as hemoglobin (Hb). Covalent binding to the N-terminal valine (Val) residue of Hb results in formation of N-(2-carbamoylethyl)valine (AAVal) and N-(2-carbamoyl-2-hydroxyethyl)valine (GAVal) Hb adducts that can be specifically cleaved off and derivatized to serve as biomarkers for long-term exposure monitoring (Bergmark et al. 1993; EFSA 2015; Fennell et al. 2005).
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