Osteoarthritis and rheumatoid arthritis are characterized by focal loss of cartilage due to an up-regulation of catabolic pathways, induced mainly by pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumour necrosis factor α (TNFα). Since reactive oxygen species are also involved in this extracellular-matrix-degrading activity, we aimed to compare the chondrocyte oxidative status responsible for cartilage damage occurring in primarily degenerative (osteoarthritis) and inflammatory (rheumatoid arthritis) joint diseases. Human articular chondrocytes were isolated from patients with osteoarthritis or rheumatoid arthritis, or from multi-organ donors, and stimulated with IL-1β and/or TNFα. We evaluated the oxidative stress related to reactive nitrogen and oxygen intermediates, measuring NO2- as a stable end-product of nitric oxide generation and superoxide dismutase as an antioxidant enzyme induced by radical oxygen species. We found that cells from patients with osteoarthritis produced higher levels of NO2- than those from patients with rheumatoid arthritis. In addition, IL-1β was more potent than TNFα in inducing nitric oxide in both arthritides, and TNFα alone was almost ineffective in cells from rheumatoid arthritis patients. We also observed that the intracellular content of copper/zinc superoxide dismutase (Cu/ZnSOD) was always lower in rheumatoid arthritis chondrocytes than in those from multi-organ donors, whereas no differences were found in intracellular manganese SOD (MnSOD) or in supernatant Cu/ZnSOD and MnSOD levels. Moreover, intracellular MnSOD was up-regulated by cytokines in osteoarthritis chondrocytes. In conclusion, our results suggest that nitric oxide may play a major role in altering chondrocyte functions in osteoarthritis, whereas the harmful effects of radical oxygen species are more evident in chondrocytes from patients with rheumatoid arthritis, due to an oxidant/antioxidant imbalance.
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Research Article|
October 26 2001
Differential roles of nitric oxide and oxygen radicals in chondrocytes affected by osteoarthritis and rheumatoid arthritis
Ilaria MAZZETTI;
Ilaria MAZZETTI
*Laboratorio di Immunologia e Genetica, Istituti Ortopedici Rizzoli, Via di Barbiano 1/10, 40136 Bologna, Italy
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Brunella GRIGOLO;
Brunella GRIGOLO
*Laboratorio di Immunologia e Genetica, Istituti Ortopedici Rizzoli, Via di Barbiano 1/10, 40136 Bologna, Italy
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Lia PULSATELLI;
Lia PULSATELLI
*Laboratorio di Immunologia e Genetica, Istituti Ortopedici Rizzoli, Via di Barbiano 1/10, 40136 Bologna, Italy
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Paolo DOLZANI;
Paolo DOLZANI
*Laboratorio di Immunologia e Genetica, Istituti Ortopedici Rizzoli, Via di Barbiano 1/10, 40136 Bologna, Italy
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Tania SILVESTRI;
Tania SILVESTRI
*Laboratorio di Immunologia e Genetica, Istituti Ortopedici Rizzoli, Via di Barbiano 1/10, 40136 Bologna, Italy
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Livia ROSETI;
Livia ROSETI
*Laboratorio di Immunologia e Genetica, Istituti Ortopedici Rizzoli, Via di Barbiano 1/10, 40136 Bologna, Italy
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Riccardo MELICONI;
Riccardo MELICONI
†Dipartimento di Medicina Interna, Cardioangiologia, Epatologia, Università degli Studi di Bologna, Via Massarenti 9, 40138 Bologna, Italy
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Andrea FACCHINI
*Laboratorio di Immunologia e Genetica, Istituti Ortopedici Rizzoli, Via di Barbiano 1/10, 40136 Bologna, Italy
‡Dipartimento di Medicina Interna e Gastroenterologia, Università degli Studi di Bologna, Via Massarenti 9, 40138 Bologna, Italy
Correspondence: Dr Andrea Facchini, Laboratorio di Immunologia e Genetica, I.O.R. (e-mail [email protected]).
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Publisher: Portland Press Ltd
Received:
January 22 2001
Revision Received:
April 27 2001
Accepted:
July 30 2001
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society and the Medical Research Society © 2001
2001
Clin Sci (Lond) (2001) 101 (6): 593–599.
Article history
Received:
January 22 2001
Revision Received:
April 27 2001
Accepted:
July 30 2001
Citation
Ilaria MAZZETTI, Brunella GRIGOLO, Lia PULSATELLI, Paolo DOLZANI, Tania SILVESTRI, Livia ROSETI, Riccardo MELICONI, Andrea FACCHINI; Differential roles of nitric oxide and oxygen radicals in chondrocytes affected by osteoarthritis and rheumatoid arthritis. Clin Sci (Lond) 1 December 2001; 101 (6): 593–599. doi: https://doi.org/10.1042/cs1010593
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