NADPH Oxidase

Publication Title: 
The Biochemical Journal

The free radical theory of aging proposes that ROS (reactive oxygen species) are major driving forces of aging, and are also critically involved in cellular senescence. Besides the mitochondrial respiratory chain, alternative sources of ROS have been described that might contribute to cellular senescence. Noxs (NADPH oxidases) are well-known sources of superoxide, which contribute to the antimicrobial capabilities of macrophages, a process involving the prototypical member of the family referred to as Nox2.

Author(s): 
Lener, Barbara
Kozie?, Rafa?
Pircher, Haymo
H¸tter, Eveline
Greussing, Ruth
Herndler-Brandstetter, Dietmar
Hermann, Martin
Unterluggauer, Hermann
Jansen-D¸rr, Pidder
Publication Title: 
Diabetes

Diabetes is a major risk factor for premature atherosclerosis, and oxidative stress appears to be an important mechanism. Previously, we showed that diabetic monocytes produce increased superoxide anion (O(2)(-)), and alpha-tocopherol (AT) supplementation decreases this. The aim of this study was to elucidate the mechanism(s) of O(2)(-) release and inhibition by AT under hyperglycemic (HG) conditions in monocytes.

Author(s): 
Venugopal, Senthil Kumar
Devaraj, Sridevi
Yang, Teddy
Jialal, Ishwarlal
Publication Title: 
Arteriosclerosis, Thrombosis, and Vascular Biology

OBJECTIVE: Excess iron may increase oxidative stress and play a role in vascular inflammation and atherosclerosis. Here we determined whether the iron chelator, desferrioxamine (DFO), ameliorates oxidative stress and cellular adhesion molecule expression in a murine model of local inflammation. METHODS AND RESULTS: Dorsal air pouches were created in C57BL/6J mice by subcutaneous injection of air. DFO (100 mg/kg body weight) was injected into the air pouch once a day for two days followed immediately on the second day by lipopolysaccharide (LPS; 2.5 mg/kg body weight).

Author(s): 
Li, Lixin
Frei, Balz
Publication Title: 
Journal of Molecular and Cellular Cardiology

C-reactive protein (CRP), a cardiovascular risk marker, induces endothelial dysfunction. We have previously shown that CRP decreases endothelial nitric oxide synthase (eNOS) expression and bioactivity in human aortic endothelial cells (HAECs). In this study, we examined the mechanisms by which CRP decreases eNOS activity in HAECs. To this end, we explored different strategies such as availability of tetrahydrobiopterin (BH4)-a critical cofactor for eNOS, superoxide (O(2)(-)) production resulting in uncoupling of eNOS and phosphorylation/dephosphorylation of eNOS.

Author(s): 
Singh, Uma
Devaraj, Sridevi
Vasquez-Vivar, Jeannette
Jialal, Ishwarlal
Publication Title: 
Journal of Cellular Physiology

Redox regulation of inducible nitric oxide synthase (iNOS) expression was investigated in lipopolysaccharide and interferon-gamma (LPS + IFNgamma)-stimulated microvascular endothelial cells from mouse skeletal muscle. Unstimulated endothelial cells produced reactive oxygen species (ROS) sensitive to inhibition of NADPH oxidase (apocynin and DPI), mitochondrial respiration (rotenone) and NOS (L-NAME). LPS + IFNgamma caused a marked increase in ROS production; this increase was abolished by inhibition of NADPH oxidase (apocynin, DPI and p47phox deficiency).

Author(s): 
Wu, Feng
Tyml, Karel
Wilson, John X.
Publication Title: 
Critical Care Medicine

OBJECTIVE: To determine the roles of nitric oxide synthase (NOS) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in the impairment of capillary blood flow in sepsis and in the reversal of this impairment by ascorbate. DESIGN: Prospective, controlled laboratory study. SETTING: Animal laboratory in research institute. SUBJECTS: Adult male wild type (WT), neuronal nitric oxide synthase (nNOS)-/-, inducible NOS (iNOS)-/-, endothelial NOS (eNOS)-/-, and gp91phox-/- mice. INTERVENTIONS: Sepsis was induced by feces injection into peritoneum (FIP).

Author(s): 
Tyml, Karel
Li, Fuyan
Wilson, John X.
Publication Title: 
Cardiovascular Research

AIMS: We investigated the mechanism by which proinflammatory stimulation induces microvascular endothelial barrier dysfunction. Since protein phosphatase type 2A (PP2A) can mediate paracellular leak and can be inactivated by tyrosine phosphorylation in its catalytic subunit (PP2Ac), we hypothesized that microvascular endothelial cells exposed to proinflammatory stimulation produce peroxynitrite that nitrates PP2Ac, and this nitration inhibits tyrosine phosphorylation of PP2Ac and thereby increases PP2A activity to mediate endothelial barrier dysfunction.

Author(s): 
Wu, Feng
Wilson, John X.
Publication Title: 
Free Radical Biology & Medicine

Reactive oxygen species (ROS) and oxidative stress are thought to play a central role in the etiology of cell dysfunction and tissue damage in sepsis. However, there is limited and controversial evidence from in vivo studies that ROS mediate cell signaling processes that elicit acute inflammatory responses during sepsis. Because NADPH oxidase is one of the main cellular sources of ROS, we investigated the role of this enzyme in lipopolysaccharide (LPS)-induced acute inflammation in vivo, utilizing mice deficient in the gp91(phox) or p47(phox) subunits of NADPH oxidase.

Author(s): 
Zhang, Wei-Jian
Wei, Hao
Frei, Balz
Publication Title: 
Arteriosclerosis, Thrombosis, and Vascular Biology

OBJECTIVE: Vascular oxidative stress and inflammation are contributing factors in atherosclerosis. We recently found that the iron chelator, desferrioxamine (DFO), suppresses NADPH oxidase-mediated oxidative stress and expression of cellular adhesion molecules in mice treated with lipopolysaccharide (LPS). The objective of the present study was to investigate whether and how LPS and iron enhance, and DFO inhibits, NADPH oxidase activity in human aortic endothelial cells (HAECs).

Author(s): 
Li, Lixin
Frei, Balz
Publication Title: 
Atherosclerosis

BACKGROUND AND OBJECTIVE: Elevated C-reactive protein (CRP) levels are associated with increased cardiovascular events and endothelial dysfunction. We have previously shown that CRP decreases endothelial nitric oxide synthase (eNOS) activity in endothelial cells and inhibits endothelium-dependent nitric oxide (NO)-mediated vasodilation in vitro. Herein, we examined the effect of in vivo administration of CRP on endothelial function and underlying mechanisms in a valid animal model.

Author(s): 
Hein, Travis W.
Singh, Uma
Vasquez-Vivar, Jeannette
Devaraj, Sridevi
Kuo, Lih
Jialal, Ishwarlal

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