Superoxide anion: Critical source of high performance antibacterial activity in Co-Doped ZnO QDs
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It is generally known that ischemic reperfusion injury is caused by cell membrane injuries due to superoxide. The present study was carried out to clarify an increase of superoxide production in human neutrophils in state of hypoxia and hyperoxia in vitro. Superoxide of neutrophils was studied at various PO2 values (air, 100% O2, 50% O2, and 100% N2 gas) by chemiluminescence method. The superoxide production (O2-) rates were 84% (air), 84% (100% N2), 87% (100% O2) and 84% (50% O2), respectively. At these stages, PO2 values were 178, 36, 764 and 370 mmHg, respectively. Since superoxide is generated in mitochondria under PO2 of 1 mmHg, it was considered that these different values of PO2 (100% N2, 100% O2 and 50% O2) do not influence the superoxide production. Other factors, such as PAF or cytokine, were speculated to increase superoxide production.
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Abstract The Bowman-Birk protease inhibitor (BBI) is a soybean-derived protease inhibitor with anticarcinogenic and anti-inflammatory properties. BBI has previously been shown to suppress the release of superoxide anion radicals from purified polymorphonuclear leukocytes. In the present study we evaluated the effect of BBI on the production of superoxide anion radicals in differentiated HL-60 cells. HL-60 cells are human lymphocytic cells that acquire neutrophil-like characteristics when treated with dimethyl sulfoxide or tetradecanoyl phorbol acetate. Superoxide anion radical production by differentiated HL-60 cells was measured in the presence of various concentrations of BBI or BBI concentrate, a soybean extract containing high levels of BBI. BBI was observed to suppress superoxide anion radical production by differentiated HL-60 cells in a dose-dependent manner. Extracts of differentiated HL-60 cells were also observed to produce superoxide anion radicals, but this activity was not affected by the presence of BBI. These results suggest that BBI inhibits superoxide anion radical generation in HL-60 cells but does not act as a simple free radical scavenger.
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The in-vitro effect of pentoxifylline, a methylxanthine derivative, on superoxide anion generation by sperm was studied in 27 men with superoxide anion production ranging from 0.57 to 13.8 nmoles 02-. per 10(6) sperm. Superoxide anion release stimulated by phorbol myristate acetate, a potent activator of oxygen radical generation, was reduced by 29-72% following the addition of 10 mM pentoxifylline. The inhibitory effect of this millimolar concentration of the drug did not depend on the initial superoxide production in the presence of phorbol myristate acetate. These results point to a potential use for pentoxifylline in the treatment of male infertility in men with an increased superoxide anion generation capacity.
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This chapter contains sections titled: C-, N-, and O-centered Radicals Si-, P-, and S-centered Radicals CC-, NN-, and OO-centered Radicals NO- and NO2-centered Radicals PO-, PP-, SO-, SS-, and SO2-centered Radicals
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Free radicals are produced by the reaction of hydroxyl radicals and amino-radicals with alkenes or halogenated alkenes. In each case the e.s.r. spectra are attributable to radicals formed by primary addition of an OH or NH2 fragment to the olefinic double bond.
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Monocyte extravasation into the vessel wall has been shown to be a critical step in the development of atherosclerosis. Upon activation, monocytes produce a burst of superoxide anion due to activation of the NADPH oxidase enzyme complex. Monocyte-derived superoxide anion contributes to oxidant stress in inflammatory sites, is required for monocyte-mediated LDL oxidation, and alters basic cell functions such as adhesion and proliferation. We hypothesize that monocyte-derived superoxide anion production contributes to atherosclerotic lesion formation. In this brief review, we summarize our current understanding of the signal transduction pathways regulating NADPH oxidase activation and related superoxide anion production in activated human monocytes. Novel pathways are identified that may serve as future targets for therapeutic intervention in this pathogenic process. The contributions of superoxide anion and NADPH oxidase to atherogenesis are discussed. Future experiments are needed to clarify the exact role of NADPH oxidase-derived superoxide anion in atherogenesis, particularly that derived from monocytes.
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