Abstract OBJECTIVE: This study investigated the 8003 base pair (bp) fragmentation damage of brain mitochondrial DNA in newborn piglets at different times after hypoxic-ischemic brain damage (HIBD) so as to explore the biomolecular foundation of neonatal neuronal metabolic disorders. METHODS: Fifty 3-day-old piglets were randomly assigned into Control and HIBD groups. The HIBD group was subdivided into groups sacrificed at 0, 24, 48 and 72 hrs post-HIBD (n=10). HIBD was induced by left carotid ligation and exposure to 8% oxygen for 2 hours. The Control group was exposed to air and was sham-operated. The left hippocampal cortexes of all subjects were obtained to amplify the fragments of 200 bp and 8003 bp by the LX-PCR method. The PCR products were electrophoresed on agaros gels to obtain the integral optical density (IOD). RESULTS: The IOD of 8003 bp fragment was markedly reduced in the HIBD 0 hr group (22.616±2.276) when compared with that of the Control group (56.995±0.317)( P<0.05). The IOD value remained lower at 24 hrs (27.719±0.309) and 48 hrs post-HIBD (49.491±3.233) (P<0.05). Until 72 hrs post-HIBD, the IOD (55.972±2.236) restored to the control value. CONCLUSIONS: The brain mitochondrial DNA was fragmented in newborn piglets following brain hypoxia-ischemia. It did not recover to normal until 72 hrs post-HIBD. The fragmentation damage of mitochondrial DNA may be related to the depression of mitochondrial respiratory enzymes activity and neuron apoptosis.
