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Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and oxidative stress is usually considered as an important factor to the pathogenesis of various diseases. Inorganic nitrite, previously viewed as a harmful substance in our diet or inert metabolites of endogenous NO, is recently identified as an important biological NO reservoir in vasculature and tissues. Stimulation of a nitrite-NO pathway shows organ-protective effects on oxidative stress and inflammation, but the mechanisms or target are not clear. In this study, the hypothesis that inorganic nitrite attenuated lipopolysaccharide (LPS)-induced oxidative stress in mice and in macrophage cells by modulating NADPH oxidase activity and NO bioavailability were investigated. We showed that nitrite treatment, in sharp contrast with the worsening effect of NO synthases inhibition, significantly attenuated aortic oxidative stress, endothelial dysfunction and mortality in LPS-induced shock in mice. Mechanistically, protective effects of nitrite were abolished by NO scavenger and xanthine oxidase inhibitor, and inhibition of NADPH oxidase with apocynin attenuated LPS-induced oxidative stress similar to that of nitrite. In the presence of nitrite, no further effect of apocynin was observed, suggesting NADPH oxidase as a possible target. In LPS-activated macrophage cells, nitrite reduced NADPH oxidase activity and oxidative stress and these effects of nitrite were also abolished by NO scavenger and xanthine oxidase inhibitor, where xanthine oxidase-mediated reduction of nitrite attenuated NADPH oxidase activity in activated macrophages via a NO-dependent mechanism. In conclusion, these novel findings position NADPH oxidase in the inflammatory vasculature as a prime target for the antioxidant effects of inorganic nitrite, and open a new direction to modulate the inflammatory response.
This article was published in the following journal.
Name: Nitric oxide : biology and chemistry
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An NADPH oxidase that is expressed by PHAGOCYTES where it transfers electrons across the plasma membrane from cytosolic NADPH to molecular oxygen on the exterior. It regulates proton (H+) flux into resting phagocytes to control intracellular pH. Mutations in the CYBB gene are associated with X-LINKED CHRONIC GRANULOMATOUS DISEASE.
A flavoprotein enzyme that catalyzes the univalent reduction of OXYGEN using NADPH as an electron donor to create SUPEROXIDE ANION. The enzyme is dependent on a variety of CYTOCHROMES. Defects in the production of superoxide ions by enzymes such as NADPH oxidase result in GRANULOMATOUS DISEASE, CHRONIC.
An NADPH oxidase that is strongly expressed in the kidney. It forms a complex with CYBA-P22PHOX and produces intracellular SUPEROXIDES that may regulate cellular signaling in APOPTOSIS; BONE RESORPTION; and NF-KAPPA B activation.
An NADPH oxidase that functions as a voltage-gated proton channel expressed by PHAGOCYTES, especially in the colon. It regulates intracellular pH, generates SUPEROXIDES upon activation by PHAGOCYTOSIS, and may play a role in INNATE IMMUNITY.
An NADPH oxidase that contains four EF HANDS and is expressed primarily by SPERMATOCYTES and LYMPHOCYTES, as well as by endothelial cells. It functions as a calcium-dependent proton channel to generate SUPEROXIDES that regulate cell growth, APOPTOSIS; and PHYSIOLOGIC ANGIOGENESIS.
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