期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 35, 期 11, 页码 1417-1430出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2003.08.009
关键词
genistein; HOCl; inflammation; oxidized LDL; free radicals
资金
- NCCIH NIH HHS [P50 AT-00477] Funding Source: Medline
- NCI NIH HHS [P30 CA13148-27] Funding Source: Medline
- NCRR NIH HHS [S10RR06487] Funding Source: Medline
- NHLBI NIH HHS [HL 58031] Funding Source: Medline
- NIAAA NIH HHS [AA12613] Funding Source: Medline
- NIEHS NIH HHS [ES/DK11504] Funding Source: Medline
Soy isoflavones and other polyphenolics have a number of potentially important beneficial effects on the pro-oxidant aspects of chronic inflammation. The impact of inflammatory cell-specific metabolism of polyphenolics, which can include halogenation and nitration, on the properties of these compounds has not been examined. Using either human neutrophils or differentiated human leukemia cells (HL-60) stimulated with phorbol ester to elicit a respiratory burst, the hypothesis that local generation of reactive oxygen and nitrogen species may metabolize and modify the biological properties of the soy isoflavones was examined. Coincubation of the stimulated cells with genistein or daidzein had no effect on the respiratory burst. Medium from stimulated cells in the presence of the isoflavones and NO2- increased the inhibition of copper-induced LDL oxidation. Mass spectrometry analysis of this medium revealed that monochlorinated, dichlorinated, and nitrated isoflavones, formed through a myeloperoxidase-dependent mechanism, were present. The consumption of genistein in the presence of cells was both extensive and rapid with > 95% of the genistein converted to either the chlorinated or nitrated metabolites within 30 min. Chemically synthesized 3'-chlorogeni stein and 3'-chlorodaidzein increased the inhibition of LDL oxidation by approximately 4-fold and 2-fold over genistein and daidzein, respectively. These results lead to the hypothesis that inflammatory cell-specific metabolism of polyphenolics can modify the properties of these compounds at the local site of inflammation. (C) 2003 Elsevier Inc.
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