Vasodilation of Tea Polyphenols Ex Vivo Is Mediated by Hydrogen Peroxide Under Rapid Compound Decay

Antioxidants

Verena Stangl¹  Karl Stangl¹  Mario Lorenz¹  Thomas Düsterhöft¹  Stephanie Lehmann²  Benno F. Zimmermann³  Ilija Djordjevic⁴ 

[1] Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Medizinische Klinik für Kardiologie und Angiologie, Campus Mitte, 10117 Berlin, Germany;Fachbereich Veterinärmedizin, Institut für Veterinär-Biochemie, Freie Universität Berlin, 14163 Berlin, Germany;Institut für Ernährungs—und Lebensmittelwissenschaften, Universität Bonn, 53115 Bonn, Germany;Klinik und Poliklinik für Herzchirurgie, herzchirurgische Intensivmedizin und Thoraxchirurgie, Universitätsklinikum Köln, 50937 Köln, Germany;

关键词: EGCG;    theaflavin;    polyphenols;    green tea;    black tea;    vasodilation;   

DOI  :  10.3390/antiox9050390

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown