China 
Africa 
Explore chapters and articles related to this topic
Health Benefits of Green Tea
Published in Robert E.C. Wildman, Richard S. Bruno, Handbook of Nutraceuticals and Functional Foods, 2019
Priyankar Dey, Geoffrey Y. Sasaki, Richard S. Bruno
Microbial metabolites of catechins that have been identified include ring fission products (e.g., valerolactones) and phenolic acids (e.g., hydroxybenzoic acids).62 These metabolites have been detected in plasma and urine of humans following green tea catechin ingestion.51,65,66 Major ring fission products include: 5-(3′,4′,5′-trihydoxyphenyl)-γ-valerolactone, 5-(3′,4′-dihydroxyphenyl)-γ-valerolactone, and 5-(3′,5′-dihydroxyphenyl)-γ-valerolactone (Figure 7.1).54,67 These metabolites are most abundant in urine, where levels reach ∼4–8 μM compared with circulating levels of ∼0.1–0.2 μM. Peak metabolite concentrations also occur several hours (5–48 h) later than those of parental catechins.36,65,66,68 If catechin bioavailability considers microbial metabolites, these metabolites represent 6%–39% of the ingested catechin dose.23
Metabolic profile elucidation of Zhi–Zi–Da–Huang decoction in rat intestinal bacteria using high-resolution mass spectrometry combined with multiple analytical perspectives
Published in Xenobiotica, 2019
Miao Wang, Qing Hu, Qingshui Shi, Gongjun Yang, Fang Feng
M6 and M9 were both metabolites related to catechins which were first observed in the 8 h-biosample. M6 gave an [M-H]– molecule ion at m/z 167.0343 and displayed product ions at m/z 335.0775, m/z 152.0115, and m/z123.0456. In view of basic fragmentation rules of MS and structural characteristics of catechin (P6), m/z 335 was supposed to be the multiple peak of [2 M-H]– while m/z 152, and m/z 123 were formed by loss of CH3 and CO2, respectively. These results were found to be identical with 2-(m,p-hydroxyphenyl)-acetic-acid, metabolite of catechin in intestinal bacteria (Goodrich and Neilson, 2014). Therefore, M6 was attributed as 2-(m,p-hydroxyphenyl)-acetic-acid. Metabolite M9 was eluted at 53.41 min and generated the deprotonated molecular ion at m/z 207.0651. Moreover, other fragments include m/z 147.0456[M-H-COOH]–, m/z 123.0453[M-H-C4H4O2]–, and m/z 105.0341[M-H-C4H4O2-H2O]– were displayed as well. As is reported, catechins can be converted into pentyl lactones under the influence of intestinal flora (Mena et al., 2017). And the fragmentation of M9 tallied with that of 5-(m,p-hydroxyphenyl)-γ-valerolactone (Sanchez-Patan et al., 2011). Thus, M9 was tentatively identified as 5-(m,p-hydroxyphenyl)-γ-valerolactone. The MS spectrogram and proposed fragmentation pathway of M9 is shown in Figure 4(c).
Extensive metabolism of flavonoids relevant to their potential efficacy on Alzheimer’s disease
Published in Drug Metabolism Reviews, 2021
Cyanidin or another metabolite protocatechuic acid, which is also a catabolite of pelargonidin, inhibited H2O2-induced mitochondrial dysfunction and DNA fragmentation, while cyanidin-3-O-β-D-glucoside did not (Tarozzi et al. 2007). In addition, protocatechuic acid inhibited Aβ aggregation and destabilized the preformed fibrils of Aβ (fAβ) in a concentration-dependent manner, and prevented PC12 cells from Aβ induced toxicity (Hornedo-Ortega et al. 2016). Caffeic acid, also a catabolite of cyanidin-3-O-β-D-glucoside, reversed memory impairment of Aβ-induced AD mice by inhibiting oxidative stress and inflammation via p38 MAPK signaling pathway (Wang et al. 2016). Apoptosis might be involved in the progress of Alzheimer’s disease, and methyl 3,4-dihydroxybenzoate, a catabolite of cyanidin-3-O-β-D-glucoside, prevented primary rat cortical neurons from Aβ-induced apoptosis by inhibiting oxidative stress and mitochondria membrane potential depolarization, and regulating apoptosis-related proteins expression, such as Bcl-2, Bax, caspase-9 and caspase-3 (Zhou et al. 2013). The ABTS radical scavenging activities of 3′,4′-dihydroxyphenyl-γ-valerolactone, 3,5-dihydroxyphenyl-γ-valerolactone and 3,5-dihydroxyphenyl-4-hydroxyvaleric acid were equal or superior to those of Trolox, although their activities accounted for one-sixth to one-third of epigallocatechin-3-O-gallate, and the arrangement of the hydroxyl groups in the phenyl group of the γ-valerolactone might determine their activities (Takagaki et al. 2011). The antioxidant ability of 3′,4′-dihydroxyphenyl-γ-valerolactone was also stronger than L-ascorbic acid, although it was about half of epicatechin (Unno et al. 2003), and it was also positively correlated with improved memory of 3 × Tg-AD mice in the novel object recognition test (Dal-Pan et al. 2017). In addition, 3,5-dihydroxyphenyl-γ-valerolactone had the same neuritogenic activity as epigallocatechin-3-O-gallate in SH-SY5Y cells (Unno et al. 2017), and the inhibitory activity of pyrogallol on acetylcholinesterase was 15.9-fold higher than its prodrug gallic acid, although both of them were inferior to their prototype epigallocatechin-3-O-gallate (Okello et al. 2012). 3-HPPA is a catabolite of apigenin-7-O-β-D-glucoside, could inhibit formation of neurotoxic Aβ aggregates and AD-type amyloid fibrils at molar ratio of 4:1 in vitro (Wang et al. 2015).