To test the scavenging of reactive oxygen species (ROS), we added synovial fluids from patients with rheumatoid arthritis (RA) and osteoarthritis, as well as hyaluronic acid (HA) and its 2 subcomponents, Dglucuronic acid and N-acetyl-D-glucosamine, to 2 ROSgenerating systems, activated neutrophils and xanthine xanthine oxidase. Synovial fluid from RA patients, HA, and D-glucuronic acid markedly decreased the 0 2 -, H,O,, OH-, and chemiluminescence measured in both systems. HA and synovial fluid, which are known to be susceptible to degradation by excessive ROS in RA patients, also seem to play an active role in protecting articular tissues from oxidative damage.Hyaluoronic acid (HA) is a glucosaminoglycan with a repeating disaccharide structure that is composed of D-glucuronic acid in / 3 1+3 linkage to Nacetyl-D-glucosamine, which in turn, is in p 1+4 linkage to the next D-glucuronic acid. HA is contained in synovial fluids as one of many proteins, proteoglycan, to which HA is bound. In the joint, HA plays an important role in the protection of articular cartilage and the transport of nutrients to cartilage (1-3). In patients with rheumatoid arthritis (RA), it has been reported that HA acts as an antiinflammatory substance by inhibiting the adherence of immune complexes to neutrophils through the Fc receptor (4), or by protecting the synovial tissues from the attachment of inflammatory mediators (5).We have previously verified that reactive oxygen species (ROS) (02-, H20,, OH-, and chemiluminescence) are generated in abundance by synovial neutrophils from RA patients, as compared with synovial neutrophils of osteoarthritis (OA) patients and peripheral neutrophils of both RA and OA patients (6). McCord (7) demonstrated that HA was susceptible to degradation by ROS in vitro, and that this could be protected by superoxide dismutase (SOD) and/or catalase, which suggests the possibility that there is pathologic oxidative damage to synovial fluid components in RA patients. Dahl et a1 (8) recently reported that there are reduced HA concentrations in synovial fluids from RA patients. It has also been reported that ROS scavengers inhibit the degradation of HA by ROS (9,101. These findings appear to support the hypothesis that ROS are responsible for the accelerated degradation of HA in the rheumatoid joint. In this study, the oxygen radical scavenging activities of synovial fluids
