Abstract:[Objective] This study clarifies the key roles of naringenin and epigallocatechin gallate (EGCG) in inhibiting 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhlP) formation in roasted meat and reveals the molecular mechanisms by which naringenin and EGCG regulate precursor consumption and intermediate accumulation, aiming to provide a scientific basis for reducing the risk of heterocyclic amines in food processing. [Method] The changes in precursors of PhIP in roasted chicken breast were determined, and a model reaction system of flavonoids, methylglyoxal (MGO), and phenylalanine (Phe) was established. The reaction kinetics curves of key substances were studied to decipher the inhibition mechanisms of naringenin and EGCG against the formation of PhlP. [Result] Naringenin and EGCG inhibited the consumption of creatine and amino acids, precursors of PhlP formation, thereby inhibiting the formation of PhlP in chicken breast during roasting. Replacing glucose (Glc) with MGO in the model reaction system helped to reduce the interference from complex reaction products, which facilitated the identification of the critical point at which naringenin and EGCG intervened in PhlP formation. Naringenin and EGCG reduced the production of the PhlP precursor phenylacetaldehyde and the Maillard reaction intermediate MGO. The reaction kinetic model data revealed that the elimination reaction rates of EGCG and naringenin with phenylacetaldehyde were the highest, indicating that the elimination reaction was a key for the two compounds in inhibiting PhlP formation. [Conclusion] EGCG and naringenin inhibited the formation of PhlP by reducing the amount of phenylacetaldehyde in the reaction system through the elimination reaction.
