The in vivo mechanism of tea polyphenol-mediated prevention of many chronic diseases is still largely unknown. Studies have shown that accumulation of toxic reactive cellular metabolites, such as ammonia and reactive carbonyl species (RCS), is one of the causing factors to the development of many chronic diseases. In our lab, we investigated the in vivo interaction between tea polyphenols including (-)-epigallocatechin 3-gallate (EGCG), theaflavin (TF), and TF-digallate (TFDG), and the deleterious reactive endogenous metabolites including ammonia and RCS. We found that EGCG could be oxidized to EGCG quinone in mice, and then rapidly react with ammonia to generate the aminated EGCG metabolite, 4'-NH2-EGCG. Both EGCG and its aminated metabolite could further scavenge RCS, such as methylglyoxal (MGO), malondialdehyde (MDA), and trans-4-hydroxy-2-nonenal (4-HNE), to produce the RCS conjugates of EGCG and the aminated EGCG in mice and in humans. In addition, we demonstrated that gut microbiota facilitate the formation of the aminated metabolite of EGCG, the RCS conjugates of EGCG, and the RCS conjugates of the aminated EGCG. Our study also demonstrated that, the major black tea polyphenols, theaflavins, could trap the endogenous metabolites including ammonia and methylglyoxal to form aminated metabolites and MGO adducts as well as their combination in mice. By exposing theaflavin to germ-free (GF) mice and specific-pathogen-free (SPF) mice, the gut microbiota was demonstrated to play an important role to mediate the amination and MGO conjugation of theaflavin. Altogether, our study provides in vivo evidences that tea polyphenols act as the house-keeping agent to scavenge toxic reactive metabolic wastes. This finding opens a new window to understand the underlying mechanisms by which drinking tea could prevent the development of chronic diseases.

Microbiota facilitates tea polyphenols to trap deleterious reactive endogenous metabolites

2019 Fall National Meeting

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