The hypothesis that aging of articular chondrocytes at a cellular level results from loss of DNA repair capability was studied by measuring unscheduled DNA synthesis (UDS). Cultured rabbit and human articular chondrocytes were irradiated with 254 nm ultraviolet light (20 J/m2) following treatment with 10 mM hydroxyurea. Neither the "in vitro senescence" nor spontaneous transformation that developed during serial passage of rabbit chondrocytes was accompanied by diminution of UDS. Synthesis of sulfated glycosaminoglycans declined more rapidly than the ability of the cells to divide. Levels of UDS by chondrocytes from old donors, rabbit or human, were comparable to those of younger individuals. UDS was greater in human than rabbit chondrocytes. Similar data have been reported previously for dermal fibroblasts but do not necessarily indicate that there is a direct or causative relationship between UDS capability and the longevity of mammalian species. X-Irradiation of rabbit chondrocytes or cartilage explants, in doses up to 40 000 rads, yielded no measurable UDS.