Green tea extract and (-)-epigallocatechin-3-gallate, the major tea catechin, exert oxidant but lack antioxidant activities.
Green tea is the most widely consumed beverage. It has attained high reputation as a health-promoting dietary component ascribed to the antioxidant activity of (-)-epigallocatechin-3-gallate (EGCG), its main polyphenolic constituent. Evidence is increasing that tea constituents can be cell damaging and pro-oxidant themselves. These effects were suggested to be due to spontaneous H2O2 generation by polyphenols in solution. In the present study, we investigated the oxidant and antioxidant properties of green tea extracts (GTE) and of EGCG by means of the rodent macrophage-like RAW 264.7 and human promyelocytic leukemic HL60 cell lines. The results obtained show that both under cell-free conditions and in the presence of cells the oxidant activities of GTE and EGCG exceeded those of spontaneously generated H2O2 (FOX assay). Increase of intracellular oxidative stress was indicated by 2',7'-dichlorofluorescin probing, and the enhanced genotoxicity was demonstrated by the alkaline comet assay and by the micronucleus assay (cytokinesis block). Time- and dose-dependent induction of cell death was monitored by trypan blue exclusion, MTT assay, and Hoechst staining. Furthermore, in our systems in vitro, EGCG neither directly scavenges H2O2 nor mediates other antioxidant activities but rather increased H2O2-induced oxidative stress and DNA damage. In conclusion, our data suggest that detailed mechanistic studies on the effects of GTE and EGCG should be performed in vivo before excessive intake and/or topical application of green tea products can be recommended to healthy and/or diseased persons.
Elbling
Leonilla
L
Institute of Cancer Research, Division of Applied and Experimental Oncology, Medical University of Vienna, Borschkegasse 8a, Vienna 1090, Austria. elbling.leonilla@meduniwien.ac.at
Weiss
Rosa-Maria
RM
Teufelhofer
Olga
O
Uhl
Maria
M
Knasmueller
Siegfried
S
Schulte-Hermann
Rolf
R
Berger
Walter
W
Micksche
Michael
M
D000111:Acetylcysteine / Q000494:pharmacology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D028241:Camellia sinensis / Q000737:chemistry*; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D002460:Cell Line; D020552:Comet Assay; D004249:DNA Damage / Q000187:drug effects; D018922:HL-60 Cells; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism / Q000494:pharmacology; D008264:Macrophages; D051379:Mice; D016877:Oxidants / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects; D010936:Plant Extracts / Q000494:pharmacology*
D000975:Antioxidants; D016877:Oxidants; D010936:Plant Extracts; D002392:Catechin; D006861:Hydrogen Peroxide; C045651:epigallocatechin gallate; D000111:Acetylcysteine