About: Effects of allopurinol on in vivo suppression of arthritis in mice and ex vivo modulation of phagocytic production of oxygen radicals in whole human blood

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About: Effects of allopurinol on in vivo suppression of arthritis in mice and ex vivo modulation of phagocytic production of oxygen radicals in whole human blood Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Effects of allopurinol on in vivo suppression of arthritis in mice and ex vivo modulation of phagocytic production of oxygen radicals in whole human blood
Creator	Graetz, Regina Kroeger, Hans Miesel, Ralf Sanocka, Dorota Zuber, Margit
source	PMC
abstract	Recently, we demonstrated elevated levels of xanthine oxidase in serum of patients with various inflammatory and autoimmune rheumatic diseases. The present study reports the antiarthritic efficacy of the xanthine oxidase inhibitor and immunosuppressant allopurinol in DBA/1xB10A(4r) mice suffering from peroxochromateinduced arthritis. A profound dose-dependent suppression of arthritis was noted (P <0.001). The ED(50) was 80±14μmol/kg/day. The arthritis index correlated positively to the phagocytic production of oxygen radicals (r (2)>0.672) and negatively to the concentration of allopurinol (r (2)=0.915). Ex vivo, allopurinol and various conventional antirheumatic drugs were screened for the inhibition of 12-otetradecanoylphorbol-13-acetate-stimulated whole human blood chemiluminescence. The concentrations of antirheumatic drugs required to inhibit the chemiluminescence by 50% were compared to the therapeutic doses administered to rheumatic patients. Whiled-penicillamine andcis-platinum(II) increased the phagocytic generation of superoxide, nonsteroidal antiinflammatory drugs (NSAIDs), steroids, and slow-acting antirheumatic drugs (SAARDs) inhibited the whole blood chemiluminescence in a dose-dependent manner. Therapeutic doses of NSAIDs, SAARDs, or steroids inhibited the phagocytic generation of reactive oxygen species by 10–50%. In addition to well-known mechanisms of action of NSAIDs and SAARDs, our results support the hypothesis that most common anti-rheumatic drugs act also by modulating the levels of reactive oxygen species, which serve important mediator and signal transduction functions in inflammatory and autoimmune diseases. Pharmacologically safe antioxidants like allopurinol, which simultaneously modify the oxidative burst of phagocytes, inhibit xanthine oxidase, and display immunosuppressive effects may well be suited to control the consequences of chronic phagocytic hyperreactivity in rheumatic patients.
has issue date	1994-01-01(xsd:dateTime)
bibo:doi	10.1007/bf01535258
bibo:pmid	7843803
has license	no-cc
sha1sum (hex)	1d474fdbea0e49794218cb044a52ee0778284acf
schema:url	https://doi.org/10.1007/bf01535258
resource representing a document's title	Effects of allopurinol on in vivo suppression of arthritis in mice and ex vivo modulation of phagocytic production of oxygen radicals in whole human blood
has PubMed Central identifier	PMC7102360
has PubMed identifier	7843803
schema:publication	Inflammation
resource representing a document's body	covid:1d474fdbea0e49794218cb044a52ee0778284acf#body_text
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