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In this study, we assessed the apoptosis induced by MIA and clarified the underlying mechanisms using the primary rat chondrocytes. The apoptosis of primary rat chondrocytes was analyzed by flow cytometry. The levels of mitochondrial membrane potential (\u0394\u03a8m) were evaluated using fluorescence spectrophotometer. The production of reactive oxygen species (ROS) was determined by fluorescence spectrophotometer. Apoptosis\u2010related protein cytochrome <jats:italic>c<\/jats:italic> and procaspase\u20103 expressions were examined by Western blotting. We found that MIA treatment induces apoptosis in chondrocytes, as confirmed by increases in the percent of apoptotic cells, up\u2010regulation of cytochrome <jats:italic>c<\/jats:italic> and caspase\u20103 protein levels. Treatment with MIA increases ROS production and decreases the levels of \u0394\u03a8m. The antioxidant, <jats:italic>N<\/jats:italic>\u2010acetylcysteine (NAC), significantly prevented the production of ROS, the reduction of \u0394\u03a8m, the release of cytochrome <jats:italic>c<\/jats:italic> and the activation of caspase\u20103. Further, NAC completely protected the cells from MIA\u2010induced apoptosis. Together these observations suggest that the mechanisms of MIA\u2010induced apoptosis are primarily via ROS production and mitochondria\u2010mediated caspase\u20103 activation in primary rat chondrocytes. \u00a9 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31: 364\u2013369, 2013<\/jats:p>","DOI":"10.1002\/jor.22250","type":"journal-article","created":{"date-parts":[[2012,11,1]],"date-time":"2012-11-01T14:48:13Z","timestamp":1351781293000},"page":"364-369","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":85,"title":["Monosodium iodoacetate induces apoptosis via the mitochondrial pathway involving ROS production and caspase activation in rat chondrocytes in 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