Abstract

Improvement of endothelial function represents a major health effect of tea in humans. Ex vivo, tea and tea polyphenols stimulate nitric oxide (NO)-dependent vasodilation in isolated blood vessels. However, it was reported that polyphenols can generate reactive oxygen species (ROS) in vitro. We therefore aimed to elucidate the role of ROS production in tea polyphenol-induced vasodilation in explanted aortic rings. Vasorelaxation of rat aortic rings was assessed in an organ chamber model with low concentrations of epigallocatechin-3-gallate (EGCG), theaflavin-3,3’-digallate (TF3), and with green and black tea, with or without pretreatment with catalase or superoxide dismutase (SOD). The stability of EGCG and TF3 was measured by HPLC, and the levels of hydrogen peroxide (H2O2) were determined. EGCG and green tea-induced vasorelaxation was completely prevented by catalase and slightly increased by SOD. TF3 and black tea yielded similar results. Both EGCG and TF3 were rapidly degraded. This was associated with increasing H2O2 levels over time. Hydrogen peroxide concentrations produced in a time range compatible with tea polyphenol decay induced NO-dependent vasodilation in aortic rings. In conclusion, tea polyphenol-induced vasodilation in vitro is mediated by low levels of H2O2 generated during compound decay. The results could explain the apparent lack of vasodilatory effects of isolated tea polyphenols in humans.

Highlights

  • Plant-derived polyphenols are widely considered as beneficial for human health [1]

  • Polyphenol-Induced Vasodilation is Prevented by Catalase but Not by superoxide dismutase (SOD)

  • Our study shows that tea polyphenol-induced vasodilation in organ bath models is characterized by a compound decay with production of hydrogen peroxide over time

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Summary

Introduction

Plant-derived polyphenols are widely considered as beneficial for human health [1]. Tea contains high amounts of polyphenols and consumption of tea has been attributed to many health-promoting effects [2,3,4]. Diseases of the cardiovascular system are alleviated by tea intake [5,6]. High consumption of tea is associated with reduced cardiovascular mortality [7,8,9] and with lower progression of atherosclerosis [10]. Especially epigallocatechin-3-gallate (EGCG), are presumed to mediate the health-promoting effects of green tea [11]. A reduction in atherosclerosis progression has been shown for green tea and EGCG in animal experiments [12,13]. Impairment of endothelial function, measured as disturbed flow-mediated dilation (FMD), is an established early

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