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Biomonitoring of nutritional acrylamide intake by consumers without dietary preferences as compared to vegans

Katharina GoerkeDivision of Food Chemistry and Toxicology, Department of Chemistry, Technische Universitaet Kaiserslautern, Erwin-Schroedinger-Straße 52, 67663, Kaiserslautern, GermanyMeike RuenzDivision of Food Chemistry and Toxicology, Department of Chemistry, Technische Universitaet Kaiserslautern, Erwin-Schroedinger-Straße 52, 67663, Kaiserslautern, GermanyAlfonso LampenDepartment of Food Safety, German Federal Institute for Risk Assessment (BfR), Max-Dohrn-Straße 8-10, 10589, Berlin, GermanyKlaus AbrahamDepartment of Food Safety, German Federal Institute for Risk Assessment (BfR), Max-Dohrn-Straße 8-10, 10589, Berlin, GermanyTamara BakuradzeDivision of Food Chemistry and Toxicology, Department of Chemistry, Technische Universitaet Kaiserslautern, Erwin-Schroedinger-Straße 52, 67663, Kaiserslautern, GermanyGerhard EisenbrandDivision of Food Chemistry and Toxicology, Department of Chemistry, Technische Universitaet Kaiserslautern, Erwin-Schroedinger-Straße 52, 67663, Kaiserslautern, GermanyElke RichlingDivision of Food Chemistry and Toxicology, Department of Chemistry, Technische Universitaet Kaiserslautern, Erwin-Schroedinger-Straße 52, 67663, Kaiserslautern, Germany. [email protected]
2019en
ABI

Annotatsiya

Acrylamide (AA) is a heat-induced food contaminant considered as genotoxic carcinogen. The present study investigated the influence of nutritional and lifestyle preferences on human AA exposure. A 10-day human study was performed with ten volunteers without nutritional preferences (omnivores) and ten vegans. Volunteers self-reported their daily routine and dietary habits. Overall mean AA intake, calculated from contents of diet duplicates, was 0.32 ± 0.19 µg/kg body weight (bw)/day with marked inter-day and inter-volunteer variabilities. Vegans ingested more AA (0.38 ± 0.23 µg/kg bw/day) than omnivore volunteers without dietary restrictions (0.26 ± 0.10 µg/kg bw/day). Excretion kinetics of urinary AA-related mercapturic acids N-acetyl-S-(2-carbamoylethyl)-L-cysteine and N-acetyl-S-(2-hydroxy-2-carbamoylethyl)-L-cysteine were essentially concordant with the respective dietary AA intake. Disproportionately enhanced AA-related biomarker excretion could be traced back to reportedly inadvertent, passive exposure to tobacco and/or fire smoke, as evidenced by the respective urinary exposure biomarkers, cotinine and N-acetyl-S-(2-cyanoethyl)-L-cysteine. Although the study is based on the comparison of small volunteer groups, the results confirm the association of AA exposure biomarkers with documented dietary preferences and lifestyle factors. Some additional contribution of endogenous background AA exposure was demonstrated individually. Disproportionately enhanced AA exposure is suggested to result from passive exposure to tobacco and/or barbecue smoke.

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