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Enhanced Lipid Peroxidation in Synoviocytes from Patients with Osteoarthritis

BRUNELLA GRIGOLO, LIVIA ROSETI, MAURO FIORINI, and ANDREA FACCHINI

ABSTRACT.

Objective.
To evaluate the degree of lipid peroxidation of synoviocytes from patients with rheumatoid arthritis (RA), osteoarthitis (OA), and controls and to look at the production of nitric oxide (NO) and its involvement in this process.

Methods. Human synoviocytes were isolated from synovial tissues from patients with RA, OA, and from healthy controls. Cells were maintained in culture for up to 3 culture passages. Lipid peroxidation, verified by the production of malonaldehyde (MDA) and 4-hydroxy-2(E)-nonenal (4-HNE), was determined by colorimetric assay. NO was evaluated by estimating the stable NO metabolite nitrite by the Griess method in the supernatants of unstimulated and interleukin (IL)-1ß and tumor necrosis factor (TNF)-a stimulated cells.

Results. Increased levels of lipid peroxidation were observed for OA-derived synoviocytes compared to RA and controls. The cells in each experimental group produced low amounts of NO both in basal and in stimulated conditions.

Conclusion. In OA, synovial cells underwent a lipid peroxidation process that did not occur in synoviocytes from RA or controls even in the absence of a detectable production of the reactive nitrogen intermediate NO. We can postulate that this peroxidation process might be due to the action of NO secreted by chondrocytes that are known to produce higher levels of this radical in OA compared to RA. (J Rheumatol 2003;30:345-7)

Key Indexing Terms:

LIPID PEROXIDATION
NITRIC OXIDE
SYNOVIOCYTES
RHEUMATOID ARTHRITIS
OSTEOARTHRITIS


From the Laboratorio di Immunologia e Genetica, Istituto di Ricerca Codivilla Putti, the Istituti Ortopedici Rizzoli, and the Dipartimento di Medicina Interna e Gastroenterologia, Università di Bologna, Bologna, Italy.

Supported by grants from Ricerca Corrente I.O.R. and Ricerca Finalizzata Ministero della Sanità, Marcatori biologici e genetici di severità dell'osteoartrosi.

B. Grigolo, PhD; L. Roseti, PhD; M. Fiorini, PhD; A. Facchini, MD, Professor of Immunology and Allergology.

Address reprint requests to Prof. A. Facchini, Laboratorio di Immunologia e Genetica, Istituto di Ricerca Codivilla Putti, I.O.R.Via di Barbiano 1/10, 40136 Bologna, Italy. E-mail: labimge@alma.unibo.it

Submitted February 26, 2002; revision accepted August 8, 2002.




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