Interaction of tea phenolics with gut microbiota may play an integral role in health benefits of these bioactive compounds, yet this interaction is not fully understood. Here, metabolic fate of epigallocatechin-3-gallate (EGCG) and its impact on gut microbiota were integrally investigated via in vitro fermentation. As revealed by UHPLC-Q-Orbitrap-MS, EGCG was promptly degraded into a series of metabolites, including 4-phenylbutyric acid, 3-(3′,4′-dihydroxyphenyl)propionic acid, and 3-(4′-hydroxyphenyl)propionic acid, through consecutive ester hydrolysis, C-ring opening, A-ring fission, dehydroxylation, and aliphatic chain shortening. Microbiome profiling indicated that, compared to the blank, EGCG treatment resulted in stimulation of the beneficial bacteria Bacteroides, Christensenellaceae, and Bifidobacterium. Additionally, the pathogenic bacteria Fusobacterium varium, Bilophila, and Enterobacteriaceae, were inhibited. Furthermore, changes in concentrations of metabolites including 4-phenylbutyric acid and phenylacetic acid, were strongly correlated with changes in abundance of specific gut microbiota. These reciprocal interactions between EGCG and gut microbiota may collectively contribute to health benefits of EGCG.

Green tea catechins are well known for their health benefits. However, these compounds can easily be oxidized, resulting in brown color formation, even in the absence of active oxidative enzymes. Browning of catechin-rich beverages, such as green tea, during their shelf life is undesired. The mechanisms of auto-oxidation of catechins and the brown products formed are still largely unknown. Therefore, we studied auto-oxidative browning of epicatechin (EC) and epigallocatechin (EGC) in model systems. Products of EC and EGC auto-oxidation were analyzed by reversed-phase ultra-high-performance liquid chromatography with photodiode array detection coupled to mass spectrometry (RP-UHPLC-PDA-MS). In the EC model system, 11 δ-type dehydrodicatechins (DhC₂s) and 18 δ-type dehydrotricatechins (DhC₃s) that were related to browning could be tentatively identified by their MS² signature fragments. In the EGC model system, auto-oxidation led to the formation of 13 dihydro-indene-carboxylic acid derivatives and 2 theaflagallins that were related to browning. Based on the products formed, we propose mechanisms for the auto-oxidative browning of EC and EGC. Furthermore, our results indicate that dimers and oligomers that possess a combination of an extended conjugated system, fused rings, and carbonyl groups are responsible for the brown color formation in the absence of oxidative enzymes.

Fortification of food with iron is considered to be an effective approach to counter the global health problem caused by iron deficiency. However, reactivity of iron with the catechol moiety of food phenolics leads to discolouration and impairs bioavailability. In this study, we investigated the interplay between intrinsic and extrinsic factors on food discolouration caused by iron-catechol complexation. To this end, a three-level fractional factorial design was implemented. Absorbance spectra were analysed using statistical methods, including PCA, HCA, and ANOVA. Furthermore, a direct link between absorbance spectra and stoichiometry of the iron-catechol complexes was confirmed by ESI-Q-TOF-MS. All statistical methods confirm that the main effects affecting discolouration were type of iron salt, pH, and temperature. Additionally, several two-way interactions, such as type of iron salt × pH, pH × temperature, and type of iron salt × concentration significantly affected iron-catechol complexation. Our findings provide insight into iron-phenolic complexation-mediated discolouration, and facilitate the design of iron-fortified foods.