We used a single-cell alkaline gel electrophoresis (SCAGE) assay to study repair of primarily single-stranded DNA breaks after in vitro exposure to ionizing radiation in cells from children with systemic lupus erythematosus (SLE), juvenile rheumatoid arthritis (JRA), systemic sclerosis (SSc) and dermatomyositis. Peripheral blood lymphocytes from patients with SLE, JRA and SSc had significantly greater DNA damage after irradiation with 1.5 Gy and 30 min incubation (i.e. repair time) than did those from controls, as assessed by the length of the migrating DNA comet. The mean comet tail lengths were: SLE, 42 microns; JRA, 40 microns; and SSc, 36 microns. Each of these was significantly different from controls, which had a mean comet tail length of 18 microns (P < 0.001, < 0.001 and < 0.05, respectively). Cells from patients with dermatomyositis had an average comet tail length of 22 microns and were not significantly different from controls. Understanding the etiology of the delay in DNA repair in these diseases may provide insight into disease pathogenesis.