Linking biomarkers of oxidative stress and disease with flavonoid consumption: From experimental models to humans

Abstract

Identification of the links among flavonoid consumption, mitigation of oxidative stress and improvement of disease in humans has significantly advanced in the last decades. This review used (−)-epicatechin (EC) as an example of dietary flavonoids, and inflammation, endothelial dysfunction/hypertension and insulin resistance/diabetes as paradigms of human disease. In these pathologies, oxidative stress is part of their development and/or their perpetuation. Evidence from both, rodent studies and characterization of mechanisms in cell cultures are encouraging and mostly support indirect antioxidant actions of EC and EC metabolites in endothelial dysfunction and insulin resistance. Human studies also show beneficial effects of EC on these pathologies based on biomarkers of disease. However, there is limited available information on oxidative stress biomarkers and flavonoid consumption to allow establishing conclusive associations. The evolving discovery of metabolites that could serve as reliable markers of intake of specific flavonoids constitutes a powerful tool to link flavonoid consumption to disease and prevention of oxidative stress in human populations.

Theaflavin 3, 3 ′ -Digallate Delays Ovarian Aging by Improving Oocyte Quality and Regulating Granulosa Cell Function

“…The natural tea polyphenol TF3 is a small molecule compound that has become increasingly popular as a dietary supplement in clinical practice; such compounds are characterized by multiple targets with naturally low toxicity or even no toxicity [ 24 ]. In this study, intragastric administration of TF3 in aged mice significantly delayed ovarian aging, as shown by maintaining ovarian reserve, shortening estrous cycle, and enlarging litter size.…”

Revisiting the Oxidation of Flavonoids: Loss, Conservation or Enhancement of Their Antioxidant Properties

“…Comparatively, lesser but still substantial evidence also exists for the ability of these compounds to exert some antioxidant actions in vivo. In fact, a number of studies in humans and animals have revealed that the increase in several markers of biological oxidation induced by ROS, such as F2-isoprostanes, hydroperoxyoctadecadienoic acids, 8-hydroxy-2′-deoxyguanosin, oxidized low density lipoprotein, nitrotyrosine and other nitrosylated or carbonylated amino acids and proteins, can be effectively prevented or ameliorated by the ingestion of certain flavonoid-rich plant foods or the administration of either flavonoid-rich extracts or pure flavonoids, as reviewed by several authors [ 46 , 47 , 48 , 49 ]. The broad recognition of the latter effects of flavonoids is likely to account for the so generalized and long perception that “flavonoids act primarily as antioxidant molecules”.…”

Supplementation with cyanidin and delphinidin mitigates high fat diet-induced endotoxemia and associated liver inflammation in mice

“…12 However, in terms of mechanisms of action, different AC display different bioactivities. 13,14 Thus, in their 3-O-glucosides forms, cyanidin and delphinidin are more efficient than other ACs like malvidin, petunidin and peonidin in attenuating tumor necrosis factor alpha (TNFα)-induced activation of the proinflammatory NF-κB signaling pathway and preventing permeabilization of Caco-2 cell monolayers, used as a model on intestinal epithelium. 15 Similarly, cyanidin and delphinidin 3-O-glucosides were more efficient than malvidin and peonidin 3-O-glucosides at stimulating glucagon-like peptide 1 (GLP-1) release from intestinal enteroendocrine cells.…”