| Literature DB >> 16488533 |
Sibylle Madlener1, Christoph Illmer, Zsuzsanna Horvath, Philipp Saiko, Annemarie Losert, Irene Herbacek, Michael Grusch, Howard L Elford, Georg Krupitza, Astrid Bernhaus, Monika Fritzer-Szekeres, Thomas Szekeres.
Abstract
Gallic acid (GA) is a naturally occurring polyhydroxyphenolic compound and an excellent free radical scavenger. In this study, we examined its cytotoxic and biochemical effects on the human HL-60 promyelocytic leukemia cell line. GA caused a significant imbalance of deoxynucleosidetriphosphate (dNTP) pool sizes, indicating ribonucleotide reductase inhibition. Moreover, GA induced dose-dependent apoptosis in HL-60 cells (80microM GA led to the induction of apoptosis in 39% of cells) and attenuated progression from G0/G1 to the S phase of the cell cycle (60microM GA doubled the number of cells in G0/G1 phase from 22 to 44% when compared to untreated controls). We further determined IC(50) values of 3.5 and 4.4nM for the inhibition of cyclooxygenases I and II, respectively. When cells were simultaneously treated with GA and trimidox, another inhibitor of RR, highly synergistic growth inhibitory effects could be observed. Taken together, we identified novel biochemical effects of GA which could be the basis for further preclinical and in vivo studies.Entities:
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Year: 2006 PMID： 16488533 DOI： 10.1016/j.canlet.2006.01.001
Source DB: PubMed Journal: Cancer Lett ISSN： 0304-3835 Impact factor: 8.679