Post-transient ischemia increase in ubiquitin conjugates in the early reperfusion.

Triton X-100-, digitonin- and urea-insoluble ubiquitin conjugates (UC) in the mitochondrial fractions of the gerbil cortex and hippocampus were analysed. In the cortex, following 5 min of forebrain ischemia, UC increased at 30 min of reperfusion and returned to the control level at 24 h. Although chronological changes in UC in the hippocampus were similar to the cortex, a more sustained increase of UC was observed. Immunoblot analysis showed that UC above 50 kDa increased in both regions. The results indicate that insoluble UC increase in the early recovery stage after ischemic neuronal damages.