Vasodilation of Tea Polyphenols Ex Vivo Is Mediated by Hydrogen Peroxide under Rapid Compound Decay
Mario Lorenz,
Stephanie Lehmann,
Ilija Djordjevic,
Thomas Düsterhöft,
Benno F. Zimmermann,
Karl Stangl,
Verena Stangl
Affiliations
Mario Lorenz
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
Stephanie Lehmann
Fachbereich Veterinärmedizin, Institut für Veterinär-Biochemie, Freie Universität Berlin, 14163 Berlin, Germany
Ilija Djordjevic
Klinik und Poliklinik für Herzchirurgie, Herzchirurgische Intensivmedizin und Thoraxchirurgie, Universitätsklinikum Köln, 50937 Köln, Germany
Thomas Düsterhöft
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
Benno F. Zimmermann
Institut für Ernährungs- und Lebensmittelwissenschaften, Universität Bonn, 53115 Bonn, Germany
Karl Stangl
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
Verena Stangl
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
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.
