Suppression of inflammatory arthritis by simultaneous inhibition of nitric oxide synthase and NADPH oxidase

Miesel, Ralf; Kurpisz, Maciej; Kröger, Hans

doi:10.1016/0891-5849(95)02026-8

Cited by 58 publications

(35 citation statements)

References 23 publications

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“…30 The latter could be of importance, as the combined inhibition of superoxide and NO was by far more effective in the treatment of experimental arthritis. 31 We did not study possible compensatory mechanisms in detail, but NO production as induced by IL-1 in synovial explants was not further increased with p47phox deficiency. We previously showed that NO derived from inducible NOS does not significantly contribute to zymosan-induced joint inflammation.…”

Section: Discussionmentioning

confidence: 99%

Deficiency of NADPH Oxidase Components p47phox and gp91phox Caused Granulomatous Synovitis and Increased Connective Tissue Destruction in Experimental Arthritis Models

Loo¹,

Bennink²,

Arntz³

et al. 2003

The American Journal of Pathology

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Recent studies indicated that the nicotinamide dinucleotide phosphate oxidase (NADPH) oxidase-derived oxygen radicals plays a deleterious role in arthritis. To study this in more detail, gonarthritis was induced in NADPH oxidase-deficient mice. Mice received an intraarticular injection of either zymosan, to elicit an irritant-induced inflammation, or poly-L-lysine coupled lysozyme, to evoke an immune-complex mediated inflammation in passively immunized mice. In contrast to wild-type mice, arthritis elicited in both p47phox ؊/؊ and gp91 ؊/؊ mice showed more severe joint inflammation, which developed into a granulomatous synovitis. Treatment with either Zileuton or cobra venom factor showed that the chemokines LTB4 and complement C3 were not the driving force behind the aggravated inflammation in these mice. Arthritic NADPH oxidase-deficient mice showed irreversible cartilage damage as judged by the enhanced aggrecan VDIPEN expression, and chondrocyte death. Neutrophils and other myeloid cells produce superoxide as part of their bacterial killing. The nicotinamide dinucleotide phosphate (NADPH) oxidase multicomponent enzyme system catalyzes the production of superoxide and the active central role plays the transmembrane cytochrome b558 which is compromised of two subunits, gp91phox and p22phox. P47phox is the cytosolic component of NADPH oxidase complex that translocates to the membrane and associates with cytochrome b556 to form the active complex that catalyzes the reduction of oxygen to superoxide at the expense of NADPH.

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Section: Discussionmentioning

confidence: 99%

Deficiency of NADPH Oxidase Components p47phox and gp91phox Caused Granulomatous Synovitis and Increased Connective Tissue Destruction in Experimental Arthritis Models

Loo¹,

Bennink²,

Arntz³

et al. 2003

The American Journal of Pathology

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“…•_ in neutrophils and monocytes from rheumatic patients positively correlate with the plasma levels of TNF- (Miesel et al, 1996). Other parameters of oxidative stress like decrease in neutrophil SOD activity and an increase in the levels of "loose" iron in the plasmalemma of RA neutrophils and monocytes were also observed (Ostrakhovitch  Afanas´ev, 2001).…”

Section: Hematopoietic Cells and Tissue As Oxidative Stress Targets Imentioning

confidence: 93%

Oxidative Stress in Human Autoimmune Joint Diseases

Škurlová¹

2012

Oxidative Stress and Diseases

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“…1993;Beckman ct a/. 1994) and arthritis (Miesel et al 1996). Peroxynitrite modifies lowdensit) lipoproteins into a form recognized by the macrophage \avenger receptor (Hogg et d. 1993).…”

Section: Potential Role Of Peroxynitrite In Various Pathophysiologicamentioning

confidence: 99%

Peroxynitrite: A Putative Cytotoxin

Demiryürek

Cakici

Kanzik

1998

Pharmacology & Toxicology

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: In recent years it has become apparent that peroxynitrite. which is one of the toxic metabolites originating from the reaction of nitric oxide and superoxide presents a number of pathologic states in which free radicals are thought to be involved. Peroxynitrite is capable of oxidizing a wide variety of biomolecules including plasma, proteins, lipids, carbohydrates and nucleic acids. Peroxynitrite is involved in the hydroxylation of aromatic compounds and acts as a nitrating agent. It modifies free or protein‐associated tyrosine residues to give nitrotyrosines, leaving a marker detectable in vivo. Peroxynitrite has been implicated in the pathophysiology of a variety of diseases including inflammation, atherosclerosis, arthritis, endotoxemia, ischaemia‐reperfusion injury, or acute respiratory distress syndrome. Development of specific peroxynitrite scavengers may provide new approaches for the effective treatment of these disease states.

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Suppression of inflammatory arthritis by simultaneous inhibition of nitric oxide synthase and NADPH oxidase

Cited by 58 publications

References 23 publications

Deficiency of NADPH Oxidase Components p47phox and gp91phox Caused Granulomatous Synovitis and Increased Connective Tissue Destruction in Experimental Arthritis Models

Deficiency of NADPH Oxidase Components p47phox and gp91phox Caused Granulomatous Synovitis and Increased Connective Tissue Destruction in Experimental Arthritis Models

Oxidative Stress in Human Autoimmune Joint Diseases

Peroxynitrite: A Putative Cytotoxin

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