Oxidative stress in rheumatoid arthritis leukocytes: suppression by rutin and other antioxidants and chelators

Citation
Ea. Ostrakhovitch et Ib. Afanas'Ev, Oxidative stress in rheumatoid arthritis leukocytes: suppression by rutin and other antioxidants and chelators, BIOCH PHARM, 62(6), 2001, pp. 743-746
Citations number
9
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Pharmacology & Toxicology
Journal title
BIOCHEMICAL PHARMACOLOGY
ISSN journal
0006-2952 → ACNP
Volume
62
Issue
6
Year of publication
2001
Pages
743 - 746
Database
ISI
SICI code
0006-2952(20010915)62:6<743:OSIRAL>2.0.ZU;2-9
Abstract
The enhanced production of superoxide ion and peroxynitrite by bloodstream neutrophils and of superoxide ion by monocytes from rheumatoid arthritis (R A) patients was registered. It was suggested that NADPH oxidase together wi th NO synthase were the major sources of superoxide ion in RA neutrophils, while in RA monocytes superoxide ion was produced by NADPH oxidase and mito chondria. Among the different free radical inhibitors studied (antioxidant enzymes, SOD and catalase; free radical scavengers, bioflavonoid rutin and mannitol; and the iron chelator desferrioxamine), SOD and rutin were the mo st efficient suppressors of oxygen radical overproduction by RA neutrophils , while mannitol and desferrioxamine were inactive. Thus, in contrast to Fa nconi anemia (FA) leukocytes (Korkina LG et al., J Leukocyte Biol 1992;52:3 57-62), iron-catalyzed hydroxyl radical formation was unimportant in RA leu kocytes, which mainly produced superoxide ion. Natural non-toxic bioflavono id rutin (vitamin P) inhibited oxygen radical overproduction in both RA and FA in an equally efficient manner and therefore may be considered as a use ful supporting pharmaceutical agent for the treatment of "free radical" pat hologies. (C) 2001 Elsevier Science Inc. All rights reserved.