In situ autolysis of mouse brain: ultrastructure of mitochondria and the function of oxidative phosphorylation and mitochondrial DNA.

The effect of in situ autolysis on cerebral mitochondrial structure and function has been investigated. Mice (n = 9) were sacrificed and stored for up to 24 h under unfavorable post-mortem conditions at 25 degrees C. At different time intervals groups of three animals were submitted to post-mortem dissection and tissue from different regions of the brain was used for the preparation of "free" and synaptosomal mitochondria. On electron microscopic examination, the post-mortem period had no significant influence on mitochondrial morphology and enzymatic activities of complexes I-V of the mitochondrial oxidative phosphorylation system were still present in all the mitochondrial preparations from different regions of the brain, albeit at a reduced levels. Degradation of mitochondrial DNA was virtually absent from mitochondrial preparations during the 24-h period of autolysis, as shown by the presence of intact DNA by Southern blot and PCR analysis. Based on these results, alterations in mitochondrial DNA and deficiencies of mitochondrial respiratory complexes I-V can be recognized in cerebral tissue even after 24 h of unfavorable post-mortem storage conditions.