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Objective. Osteoarthritis (OA) is a degenerative rheumatic disease that is associated with extracellular matrix degradation and chondrocyte apoptosis in the articular cartilage. The role of mitochondria in degenerative diseases is widely recognized. We undertook this study to evaluate mitochondrial function in normal and OA chondrocytes and to examine age-related changes in mitochondria.Methods. Mitochondrial function was evaluated by analyzing respiratory chain enzyme complexes and citrate synthase (CS) activities as well as changes in mitochondrial membrane potential (⌬⌿m). The activities of mitochondrial respiratory chain complexes (complex I: rotenone-sensitive NADH-coenzyme Q 1 reductase; complex II: succinate dehydrogenase; complex III: antimycin-sensitive ubiquinol cytochrome c reductase; and complex IV: cytochrome c oxidase) and CS were measured in human articular chondrocytes isolated from OA and normal cartilage. ⌬⌿m was measured by JC-1 using flow cytometry. Statistical analysis was performed using the Mann-Whitney U test and Student's t-test as well as several models of multiple linear regression.Results. OA articular chondrocytes had reduced activities of complexes II and III compared with cells from normal cartilage. However, the mitochondrial mass was increased in OA. Cultures of OA chondrocytes contained a higher proportion of cells with de-energized mitochondria. We found no relationship between mitochondrial function and donor age either in normal or in OA chondrocytes. Conclusion. These findings suggest the involvement of mitochondrial function in the pathophysiology of OA. Cartilage degradation by OA and cartilage aging may be two different processes.Osteoarthritis (OA) is a degenerative joint disease that is characterized by articular cartilage degradation. The final phase of OA seems to reflect a failure of the reparative process, resulting in degradation of the matrix, cell death, and total loss of cartilage integrity. The chondrocyte is the only cell type that is present in mature cartilage, and it is responsible for repairing the damaged tissue (1,2).Mitochondria are complex organelles that oxidize a wide range of metabolic intermediates. It has been reported that in living cells, these organelles have a characteristic appearance that depends on the tissue type and the oxidative state of the cell. Multienzyme complexes located both in the inner mitochondrial membrane and in the mitochondrial matrix oxidize tricarboxylic acid-cycle intermediates derived from primary nutrients. ATP is generated by the activity of an electrogenic proton pump that spans the inner mitochondrial membrane. The energy for synthesis of ATP is derived from two components: a pH gradient and the electric potential across the mitochondrial membrane.Mitochondrial impairment and defective oxidative phosphorylation have been linked to some human disorders (3,4). Mitochondria are important in regulating cell survival (5-9), and the classic signs of cell death

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