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Epigallocatechin gallate protects U937 cells against nitric oxide‐induced cell cycle arrest and apoptosis
Author(s) -
Kelly Melissa R.,
Geigerman Cissy M.,
Loo George
Publication year - 2001
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.1097
Subject(s) - apoptosis , cell cycle , nitric oxide , s nitrosoglutathione , chemistry , annexin , population , epigallocatechin gallate , u937 cell , cell , peroxynitrite , cell cycle checkpoint , biochemistry , microbiology and biotechnology , biology , superoxide , antioxidant , polyphenol , medicine , glutathione , environmental health , organic chemistry , enzyme
Ingesting phenolic phytochemicals in many plant products may promote health, but the effects of phenolic phytochemicals at the cellular level have not been fully examined. Thus, it was determined if the tea phenolic phytochemical, epigallocatechin gallate (EGCG), protects U937 human pro‐monocytic cells against the nitrogen free radical, nitric oxide (•NO). Cells were incubated for 4–6 h with 500 μM S‐nitrosoglutathione (GSNO), which generates •NO, but this did not induce single‐strand breaks in DNA. Nevertheless, 82 ± 4% of GSNO‐treated cells, compared to only 39 ± 1% of untreated cells, were arrested in the G 1 ‐phase of the cell cycle. However, dosing the GSNO‐treated cells with 9, 14, or 18 μg/ml of EGCG resulted in only 74 ± 8%, 66 ± 1%, and 43 ± 3% of the cells, respectively, in the G 1 ‐phase. Exposing cells to GSNO also resulted in the emergence of a sub‐G 1 apoptotic cell population numbering 14 ± 3%, but only 5 ± 2%, 5 ± 1%, and 2 ± 0% upon dosing of the GSNO‐treated cells with 9, 14, and 18 μg/ml of EGCG, respectively. Furthermore, exposing cells to GSNO resulted in greater cell surface binding of annexin V‐FITC, but binding was 41–89% lower in GSNO‐treated cells dosed with EGCG. Collectively, these data suggest that •NO or downstream products induced cell cycle arrest and apoptosis that was not due to single‐strand breaks in DNA, and that EGCG scavenged cytotoxic •NO or downstream products, thus reducing the number of cells in a state of cell cycle arrest or apoptosis. J. Cell. Biochem. 81: 647–658, 2001. © 2001 Wiley‐Liss, Inc.