No abstract

The accumulation of heterocyclic amines (HAs) and advanced glycation end products (AGEs) during different processing stages was investigated in commercial raw materials to plant-based hamburger meats (PBHMs). Principal component analysis (PCA) was performed to explore the difference between the samples of each processing stage. The total free HA level accumulated from 4.74–6.63 ng/g in raw plant proteins to 5.81–20.23 ng/g in textured vegetable proteins after extrusion. The concentration of MeAαC increased from 29.23 ± 3.50 to 59.44 ± 0.26 ng/g, resulting in an accumulation of the total protein-bound HAs after cooking at 160 °C for 6 min, but the MeAαC content decreased to 42.26 ± 0.11 ng/g when the heating duration was prolonged to 12 min. An evident accumulation of AGEs was observed during the thermal home-processing of PBHM. The total levels for all HAs were 381.30 and 160.30 ng/g in roast beef patty (RBP) and PBHM, respectively, with RBP having a better amino acid composition pattern. These results may reveal the target processing stage, which should be paid attention to for the inhibition of Maillard reaction derivative harmful products (MRDHPs) in plant-based meat products.

Although various inhibitors have been employed to react with phenylacetaldehyde to form adducts and thus interrupt the formation of 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine (PhIP), high concentrations of PhIP remain in the final system. It remains unknown whether other critical aldehyde or ketone intermediates are involved in the generation of PhIP, and scavenging these reactive carbonyls simultaneously may achieve higher inhibitory efficiency of PhIP. In this study, reactive carbonyls in a glucose/creatinine/phenylalanine model system were first identified by gas chromatography−mass spectrometry (GC−MS), and then the single and synergistic effects of nonprecursor amino acids (cysteine, methionine, proline, histidine, arginine, and leucine) on scavenging reactive carbonyls were investigated to find out promising combination partners. The obtained results showed that the concentrations of benzaldehyde and phenylacetaldehyde in the glucose/creatinine/phenylalanine model system reached 0.49 ± 0.01 and 6.22 ± 0.21 μg/mL, respectively. Heating these carbonyl compounds in the presence of creatinine resulted in the quantity of PhIP produced increasing linearly with the added quantity of benzaldehyde (r = 0.9733, P = 0.0002) and phenylacetaldehyde (r = 0.9746, P = 0.0002), indicating that both compounds are key intermediates for PhIP generation. Among the investigated amino acids, histidine produced the maximum inhibition of PhIP formation (78−99%) in the benzaldehyde/creatinine model system, and proline produced the maximum inhibition of PhIP formation (13−97%) in the phenylacetaldehyde/creatinine model system, where both compounds decreased PhIP formation in a dose-dependent manner. Histidine in combination with proline enhanced the inhibitory effect against PhIP formation at a low addition level, where the highest inhibitory efficiency was obtained using a 1:3 mass ratio of histidine to proline (2 mg/mL in total), reducing PhIP formation by 96%. These findings suggest that histidine−proline combinations can scavenge benzaldehyde and phenylacetaldehyde simultaneously, enhancing the suppression of PhIP formation.