The Respiratory Burst Oxidase

Babior, Bernard M.

doi:10.1002/9780470123119.ch2

Cited by 99 publications

(17 citation statements)

References 234 publications

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“…When stimulated by extracellular signals, such as hormones, cytokines and even bacteria, p47phox, p67phox, p40phox and Rac in the cytoplasm bind to p22phox through its proline-rich tail and form the enzyme complex. Such binding leads to conformational changes of gp91phox, and activates the enzyme by inducting transmembrane electron transportation, thereby fulfilling its biological roles [7,8].…”

Section: Discussionmentioning

confidence: 99%

“…In addition to its involvement in host defense, ROS serves as a secondary messenger participating in the regulation of cell differentiation, proliferation and apoptosis. The homolog family of NADPH oxidase found in the plasma membrane of non-phagocytic cells, which was later named the NOX protein family, provides direct evidence for the production and function of ROS in non-phagocytic cells [7,8].…”

Section: Introductionmentioning

confidence: 99%

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Expression and clinical significance of non-phagocytic cell oxidase 2 and 4 after human traumatic brain injury

Tian

Zhong

et al. 2014

Neurol Sci

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The goal of this study was to examine NOX2 and NOX4 expression in clinical samples of patients with traumatic brain injury (TBI), and to explore the correlation of NOX2 and NOX4 expression with the severity of injury, duration of injury, and prognosis. Brain samples of 20 TBI patients within 1 cm of the contusion site were collected and grouped based on duration of injury, Glasgow Coma Scale (GCS) and Glasgow Outcome Scale (GOS), and immunofluorescence staining were performed to examine the expression levels of NOX2 and NOX4 in the neurons and astrocytes. We found that the expression level of NOX2 in neurons and positive rate of NOX2 expression in astrocytes peaked at 12-24 and 6-12 h after injury, respectively. The expression level of NOX4 in neurons peaked at 24-48 h, and the positive rate of NOX4 expression gradually increased with prolonged injury. We also found that the higher the GCS score, the lower the expression levels of NOX2 and NOX4 in neurons was, while higher the GCS score, the lower the positive rate of NOX4 expression in astrocytes was and the higher the GOS grade, the lower the positive rate of expression in astrocytes was. In conclusion, NOX2 and NOX4 expressions significantly increase at an early stage after TBI, and abnormal expressions of NOX2 and NOX4 are correlated to patient prognosis to certain extent.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Expression and clinical significance of non-phagocytic cell oxidase 2 and 4 after human traumatic brain injury

Tian

Zhong

et al. 2014

Neurol Sci

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“…ROS such as super oxide anion (O 2 − ), hydrogen peroxide (H 2 O 2 ), and the hydrogen radical (OH ⋅ ) are generated in vivo from exposure to environmental agents such as radiation and redox cycling agents [11]. Oxidative stress occurs when the production of ROS exceeds the body's natural antioxidant defense mechanisms, causing damage to macromolecules, such as DNA, proteins, and lipids [12].…”

Section: Introductionmentioning

confidence: 99%

Lead and Cadmium Co-exposure Mediated Toxic Insults on Hepatic Steroid Metabolism and Antioxidant System of Adult Male Rats

Pandya

Pillai

Gupta

2009

Biol Trace Elem Res

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The redox status and steroid metabolism of liver of adult male rat exposed to lead (Pb) and cadmium (Cd) either alone or in co-exposure (0.025 mg/kg body weight intraperitoneally/15 days) was studied. Pb and Cd significantly accumulated in the liver. The activity of steroid metabolizing enzymes 17-betahydroxysteroid oxidoreductase and uridine diphosphate-glucuronyltransferase were decreased in experimental animals. 17-beta-Hydroxysteroid dehydrogenase was reduced to 33%, 38%, and 24% on treatment of Pb, Cd, and co-exposure (Pb + Cd). Furthermore, the activity of uridine diphosphate-glucuronosyltransferase was significantly reduced to 27% (Pb exposure), 36% (Cd exposure), and 25% (co-exposure of Pb + Cd). Cd exposure exhibited more toxic effect than Pb, while co-exposure demonstrated the least. The activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione reductase, and glucose-6-phosphate dehydrogenase decreased and glutathione peroxidase increased in mitochondrial and post-mitochondrial fractions. The level of lipid peroxidation increased, and cellular glutathione concentration decreased. Hepatic DNA was decreased, whereas RNA content and the activity of alanine transaminase remained unchanged. Histological studies revealed that only Cd-exposed groups exhibited cytotoxic effect. These results suggest that when Pb and Cd are present together in similar concentrations, they exhibited relatively decreased toxic effect when compared to lead and cadmium in isolation with regard to decreased steroid metabolizing and antioxidant enzyme activities. This seems that the toxic effect of these metals is antagonized by co-exposure due to possible competition amongst Pb and Cd for hepatic accumulation.

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“…One of the key mechanisms is the production of reactive oxygen species (ROS), which relies on the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex [14]. In resting cells, the NADPH oxidase is unassembled and inactive, with several protein components segregated into membrane (gp91 phox and p22 phox ) and cytosolic (p47 phox , p67 phox , p40 phox , and Rac2) locations [15,16].…”

Section: Introductionmentioning

confidence: 99%

TLR2 enhances NADPH oxidase activity and killing of Staphylococcus aureus by PMN

Jann¹,

Schmaler²,

Ferracin³

et al. 2011

Immunology Letters

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The Respiratory Burst Oxidase

Cited by 99 publications

References 234 publications

Expression and clinical significance of non-phagocytic cell oxidase 2 and 4 after human traumatic brain injury

Expression and clinical significance of non-phagocytic cell oxidase 2 and 4 after human traumatic brain injury

Lead and Cadmium Co-exposure Mediated Toxic Insults on Hepatic Steroid Metabolism and Antioxidant System of Adult Male Rats

TLR2 enhances NADPH oxidase activity and killing of Staphylococcus aureus by PMN

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