The main catechin of green tea, (−)-epigallocatechin-3-gallate (EGCG), reduces bleomycin-induced DNA damage in human leucocytes
Interest in the beneficial effects of green tea has led to investigations on activities by the main catechin (−)-epigallocatechin-3-gallate (EGCG). This antioxidative compound could contribute to cancer chemoprevention by acting antigenotoxic. To further explore this hypothesis we investigated antig...
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Veröffentlicht in: | Toxicology in vitro 2006-04, Vol.20 (3), p.295-300 |
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Sprache: | eng |
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Zusammenfassung: | Interest in the beneficial effects of green tea has led to investigations on activities by the main catechin (−)-epigallocatechin-3-gallate (EGCG). This antioxidative compound could contribute to cancer chemoprevention by acting antigenotoxic. To further explore this hypothesis we investigated antigenotoxic potentials of low EGCG concentrations in human peripheral leucocytes. Leucocytes isolated from whole blood were (1) stimulated with phytohaemagglutinin, (2) damaged with genotoxic bleomycin, and (3) post-incubated to allow DNA repair. After each phase DNA integrity was measured with the comet assay. EGCG (2, 20, 100
μM) was added either during phases 1, 2 or 3 or during the whole process (1–3), to delineate mechanisms of antigenotoxicity reflecting induction of detoxification (phase 1), scavenging of radicals (phase 2), stimulation of repair (phase 3), respectively. Bleomycin induced breaks and endonuclease III specific damage, but EGCG did not affect damage or repair of these lesions when added during phases 1, 2 or 3. However, the application of EGCG during phases 1 and 2 significantly reduced both bleomycin-induced breaks and endonuclease III sensitive sites. EGCG added during all phases impaired persistence of damage. Our studies show that the continuous presence of EGCG can reduce radical-induced DNA damage in primary leucocytes, possibly due to a combination of different mechanisms. Together the findings support the hypotheses that EGCG acts protective in human cells. |
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ISSN: | 0887-2333 1879-3177 |
DOI: | 10.1016/j.tiv.2005.08.002 |