Bjellaas Thomas, Olesen Pelle T, Frandsen Henrik, Haugen Margaretha, Stølen Linn H, Paulsen Jan E, Alexander Jan, Lundanes Elsa, Becher Georg
Division of Environmental Medicine, Norwegian Institute of Public Health, Nydalen, NO-0403 Oslo, Norway.
Toxicol Sci. 2007 Jul;98(1):110-7. doi: 10.1093/toxsci/kfm091. Epub 2007 Apr 21.
In a study comprising 50 subjects, we investigated the relationship between acrylamide (AA) intake from food using food frequency questionnaires and the concentration of hemoglobin (Hb) adducts of AA and its genotoxic metabolite glycidamide (GA) as a measure of the internal exposure. A method using solid-phase extraction and liquid chromatography with negative electrospray tandem mass spectrometric (MS/MS) detection for the determination of the Hb adducts as phenylthiohydantoin derivatives in human blood was developed. The limit of quantification for AA- and GA-Hb adducts were 2 and 6 pmol/g globin, respectively, and the between-assay precision was below 25%. The estimated dietary intake of AA was (median and range) 13.5 microg/day (4.1-72.6) in nonsmokers and 18.3 microg/day (7.8-32.0) in smokers. In nonsmokers, males had a higher intake than females, 16.6 microg/day (18.6-72.6) and 12.8 microg/day (4.1-30.2), respectively. Nonsmokers had a median AA and GA adduct concentration of 36.8 (range 17.9-65.5) and 18.2 (range 6.7-45.6) pmol/g globin, respectively. In smokers, the values were 165.8 (98.8-211) and 83.2 (29.1-99.0) pmol/g globin, respectively. Using multiple linear regression analysis, a significant positive correlation was found between the AA-Hb adduct concentration and the intake of chips/snacks and crisp bread. GA-Hb adduct did not correlate with consumption of any of the main food groups. Neither AA-Hb nor GA-Hb adduct concentration correlated with total dietary intake of AA as calculated from the reported food intake. Adduct concentrations did not correlate with 24 h urinary excretion of mercapturic acid metabolites of AA and GA in the same subjects reported previously.
在一项包含50名受试者的研究中，我们使用食物频率问卷调查了食物中丙烯酰胺（AA）的摄入量与AA血红蛋白（Hb）加合物及其遗传毒性代谢物缩水甘油酰胺（GA）的浓度之间的关系，以此作为体内暴露的一种衡量指标。我们开发了一种使用固相萃取和液相色谱结合负电喷雾串联质谱（MS/MS）检测的方法，用于测定人血中作为苯硫代乙内酰脲衍生物的Hb加合物。AA-Hb和GA-Hb加合物的定量限分别为2和6 pmol/g珠蛋白，批间精密度低于25%。非吸烟者AA的估计膳食摄入量（中位数和范围）为13.5μg/天（4.1 - 72.6），吸烟者为18.3μg/天（7.8 - 32.0）。在非吸烟者中，男性摄入量高于女性，分别为16.6μg/天（18.6 - 72.6）和12.8μg/天（4.1 - 30.2）。非吸烟者AA和GA加合物浓度的中位数分别为36.8（范围17.9 - 65.5）和18.2（范围6.7 - 45.）pmol/g珠蛋白。在吸烟者中，这些值分别为165.8（98.8 - 211）和83.2（29.1 - 99.0）pmol/g珠蛋白。使用多元线性回归分析发现，AA-Hb加合物浓度与薯片/零食和脆面包的摄入量之间存在显著正相关。GA-Hb加合物与任何主要食物组别的摄入量均无相关性。AA-Hb和GA-Hb加合物浓度与根据报告的食物摄入量计算出的AA总膳食摄入量均无相关性。加合物浓度与先前报告的同一受试者中AA和GA的硫醚氨酸代谢物的24小时尿排泄量无相关性。
