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Chain breaking antioxidant status in rheumatoid arthritis: clinical and laboratory correlates

Authors :
Situnayake, R.D.
Thurnham, D.I.
Kootathep, S.
Chirico, S.
Lunec, J.
Davis, M.
McConkey, B.
Source :
Annals of the Rheumatic Diseases. Feb, 1991, Vol. 50 Issue 2, p81, 6 p.
Publication Year :
1991

Abstract

Rheumatoid arthritis (RA) is a disease that causes inflammation of the joints. During the process of inflammation, oxygen radicals (highly reactive atoms with unpaired electrons) are generated within the joint tissue. When samples of joint tissue are grown in culture and oxygen radicals are added, the radicals damage (oxidize) and destroy the joint tissue. In this way, oxygen radicals are thought to be involved in RA. Under normal circumstances, the body makes its own proteins, called antioxidants, that inactivate oxygen radicals and prevent them from causing tissue damage. These antioxidants include specific enzymes and vitamins E and C (ascorbic acid). In order to investigate the relationship between oxygen radicals and RA, blood samples from 20 patients with RA and 20 healthy volunteers were tested for the presence of antioxidants. The levels of antioxidants (vitamin E, ascorbic acid and urate) present in the blood samples were determined by measuring the amount of protein damage that occurred following the addition of oxygen radicals to the blood. The patients with RA had lower blood levels of antioxidants than those without RA. Lower blood levels of antioxidants appeared to be related to morning joint stiffness, pain and grip strength. Also, the blood samples that contained high levels of urate were less susceptible to damage by oxygen radicals. These findings indicate that patients with RA are more susceptible to tissue damage caused by oxygen radicals than people who do not have RA. (Consumer Summary produced by Reliance Medical Information, Inc.)

Details

ISSN :
00034967
Volume :
50
Issue :
2
Database :
Gale General OneFile
Journal :
Annals of the Rheumatic Diseases
Publication Type :
Periodical
Accession number :
edsgcl.10593235