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[An experimental study on large fragment deletion of rat myocardial mitochondrial DNA during early postburn stage]
Dong-xia Zhang1, Yue-sheng Huang, Song-tao Zhao
1Institute of Burn Research, Southwest Hospital, State Key Laboratory of Trauma, Burns and Combined Injury, The Third Military Medical University, Chongqing 400038, P.R. China.
Objective:
To investigate the influence of peroxidative injury in rat myocardium on the mitochondrial DNA (mtDNA) during early postburn stage.
Methods:
Thirty-six Sprague-Dawley (SD) rats were employed in the study and were randomly divided into sham scald (SS) and scald groups. The rats in scald groups were inflicted with 30% TBSA III degree scalding and were further divided into 1, 3, 6, 12 and 24 post-scald hour (PSH) groups. The mtDNA deletion was determined by semi-quantitative PCR. The rat myocardial tissue samples were harvested and homogenized and the contents of superoxide dismutase (SOD) and malondialdehyde (MDA) were determined.
Results:
There was no mtDNA deletion in the rat myocardium in SS group. Partial or complete large fragment (4.8 kb) mtDNA deletion in the rat myocardium was identified at 1, 3 and 24 PSHs (P < 0.05 or 0.01). The SOD activity in the rat myocardium significantly decreased at 1 PSH, reaching the lowest level (76.90 +/- 8.30 U/mg) at 6 PSH, but the MDA content increased evidently at 1 PSH, peaking [(3.17 +/- 0.80) nmol/mg] at 6 PSH (P < 0.05).
Conclusion:
Peroxidative injury to the rat myocardium during early postburn stage might be the principal cause of the 4834 bp deletion of mtDNA in rat myocardium.
