Insoluble ubiquitin conjugates (UC) in the mitochondrial fraction of the gerbil cortex were analyzed following transient forebrain ischemia. At 1 h of reperfusion after 2-10 min of ischemia, UC increased as the duration of ischemia was prolonged. Pre-treatment with pentobarbital, rather than post-treatment immediately after recirculation, reduced the increase of UC at 1 h of reperfusion following 5 min of ischemia. Pentobarbital had no effect on in vitro ubiquitination of heat-denatured lysozyme by the extract of gerbil cortex. These results suggest that increase in UC is dependent on ischemic damage and pentobarbital attenuates the increase of UC by relieving injury during ischemia.
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