Using an in situ nick translation procedure, DNA single-strand breaks (SSB) in postischemic gerbil hippocampus were investigated after 15-min forebrain ischemia followed by 0-4h of recirculation. In the control group, increased SSB were noticed in the ependymal cell layer and the dentate gyrus. After 15-min ischemia without recirculation, no remarkable changes in SSB were observed. However, after 1 h of recirculation, a marked increase in SSB was recognized throughout the hippocampus, especially in the cells in CA1 subfield and the dentate gyrus. After 4 h of recirculation, SSB decreased to a level near that of the control group. The results of the present study indicate that ischemic insults may injure intranuclear DNA during postischemic recirculation periods. Although many factors may be involved, activated endonuclease due to an intracellular Ca2+ rise, free radicals, and postischemic hyperthermia appear to be involved in this phenomenon.