The effect of acrolein on the formation of the 2-amino-1-methyl-6-phenylimidazo[4,5- b ]pyridine (PhIP) was investigated in a chemical model. Acrolein was found to increase PhIP formation at each tested addition level. 0–0.2 mmol of acrolein increased PhIP formation dose-dependently, while high levels of acrolein (>0.2 mmol) did not further increase PhIP formation. Mechanistic study showed that acrolein addition decreased the residue of phenylalanine and creatinine, but increased the content of some key intermediates. Further analysis indicated that acrolein can react with phenylalanine, creatinine, and PhIP to form adducts. These results suggested that acrolein was able to contribute to PhIP formation as a consequence of its comprehensive ability to facilitate Strecker degradation of phenylalanine and react with phenylalanine, creatinine, and PhIP. In addition, oxidation of the tilapia fish increased the PhIP formation in the roasted fish patties, further supporting the potential contribution role of lipid oxidation products to the formation of PhIP.
Ya Jiang,Qingqing Jiang,Daming Fan,Mingfu Wang,Yueliang Zhao
The effect of acrolein, a lipid oxidation product, on the formation of the heterocyclic aromatic amine 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) was investigated in a chemical model containing glycine, creatinine, and glucose. Acrolein addition at 0.02–0.2 mmol increased MeIQx formation, while high levels of acrolein (>0.2 mmol) did not further increase MeIQx formation. Moreover, acrolein addition decreased the residue of glycine and creatinine but increased the residue of glucose; it also increased the formation of volatile intermediates in the MeIQx-producing chemical model. Further analysis indicated that acrolein can react with glycine, creatinine, and MeIQx to eliminate them. These results revealed that acrolein was able to contribute to MeIQx formation as a consequence of the comprehensive ability of acrolein to facilitate Strecker degradation of glycine, increase the formation of volatile intermediates, and react with glycine, creatinine, and MeIQx. In addition, the oxidation of minced salmon increased the content of MeIQx in the roasted salmon patties, further supporting the potential contribution role of lipid oxidation products in the formation of MeIQx.
The inhibitory effects of four hydrocolloids, including alginic acid, pectin, carboxymethylcellulose sodium salt, and chitosan on the formation of two typical toxic advanced glycation end products N Ɛ -(carboxymethyl) lysine (CML) and N Ɛ -(carboxyethyl) lysine (CEL) were investigated in chemical models and fish patties. All the four hydrocolloids were found to significantly inhibit CML and CEL formation in chemical models, and among them, pectin and alginic acid were the most effective inhibitors. In roast fish patties, the addition of pectin and alginic acid at 0.9% reduced the content of CML by 43.6% and 44.9%, and CEL by 32.4% and 32.6%, respectively. Moreover, alginic acid plus a polyphenol epigallocatechin gallate (EGCG) showed stronger inhibitory effect against CML and CEL formation than alginic acid alone. Further study showed that alginic acid and pectin decreased the formation of glyoxal (GO) and methylglyoxal (MGO), two key intermediates of CML and CEL, in the chemical models and fish patties. In addition, compared with EGCG, the addition of alginic acid in fish patties showed less impact on color, odor, and sensory properties. These findings suggest that alginic acid is a potent inhibitor against the formation of AGEs with less impact on food quality.
危险品化学品经营许可证（带存储）