Green tea extract and its polyphenols markedly inhibit luminol-dependent chemiluminescence activated by peroxynitrite or SIN-1.
This study is based on a simple chemical interaction of peroxynitrite (OONO-) and luminol, which produces blue light upon oxidation. Since peroxynitrite has a half-life of less than 1 s, a drug known as SIN-1 is used as a peroxynitrite generator. In addition peroxynitrite itself was used directly with a fast injection-mixing system to ascertain whether there are differences between it and the peroxynitrite-generating system (SIN-1) which mimics the natural production of (OONO-). Peroxynitrite is a potent oxidizing compound (1000 times more active than equidose hydrogen peroxide) and it can oxidize carbohydrates, lipids, proteins and nucleic acids. Upon stimulation by inflammation and/or infection, macrophages and neutrophils can be activated to produce large amounts of peroxynitrite. We are interested in simple chemicals that are non-toxic that could inhibit or destroy peroxynitrite, which might otherwise cause inappropriate damage to blood and tissues. Green tea is a complex mixture containing several potent major antioxidant constituents, eg flavins and/or polyphenols. The constituents in green tea may react directly or indirectly with peroxynitrite or its constituents through the process of antioxidation to inhibit light. Alternatively, compounds could produce superoxide which, when reacted with nitric oxide, could produce more peroxynitrite and hence more light with luminol. Therefore, as the tea or antioxidants from tea are diluted, while the peroxynitrite or its precursors are kept at a constant concentration, one can observe unusual behaviour regarding light emission. Initially, at high doses of tea or antioxidant, one observes clear inhibition of the light generated from the reaction of peroxynitrite and luminol. However, at dilute concentrations of antioxidants, one can often observe stimulation of light. Possible reasons for these observations are discussed.
Van Dyke
K
K
Department of Pharmacology and Toxicology and Genetics/Developmental Biology, Robert C. Byrd Health Sciences Center and West Virginia University Medical School, Morgantown, West Virginia 26506, USA. kvandyke@hsc.wvu.edu
McConnell
P
P
Marquardt
L
L
D002392:Catechin / Q000031:analogs & derivatives / Q000737:chemistry*; D005419:Flavonoids; D007700:Kinetics; D008163:Luminescent Measurements; D008165:Luminol / Q000737:chemistry*; D008981:Molsidomine / Q000031:analogs & derivatives* / Q000737:chemistry; D009566:Nitrates / Q000737:chemistry*; D020030:Nitric Oxide Donors / Q000737:chemistry*; D016877:Oxidants / Q000737:chemistry*; D010084:Oxidation-Reduction; D010636:Phenols / Q000737:chemistry*; D010936:Plant Extracts; D011108:Polymers / Q000737:chemistry*; D013662:Tea
D005419:Flavonoids; D009566:Nitrates; D020030:Nitric Oxide Donors; D016877:Oxidants; D010636:Phenols; D010936:Plant Extracts; D011108:Polymers; D013662:Tea; C039642:peroxynitric acid; D008165:Luminol; C002385:linsidomine; D002392:Catechin; C062669:epicatechin gallate; C045651:epigallocatechin gallate; D008981:Molsidomine