<Originals>Pathophysiological characteristics of mitochondria and structural abnormality of mitochondrial DNA in hypertrophied myocardium of stroke-prone SHR
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To clarify the importance of mitochondrial alteration for pathogenesis in stroke-prone SHR (SHRSP) hypertrophied heart, morphological and biochemical changes in isolated mitochondria were examined at prehypertensive and hypertensive stages, in comparison with those in Wistar-Kyoto rats (WKY). Furthermore, the structural alteration in mitochondrial DNA (mtDNA) was examined by restriction fragment length polymorphism (RFLP) analysis. At 5 weeks of age (prehypertensive stage), although the blood pressure of SHRSP was already higher than that of WKY, no significant differences were found in any parameters examined in the present study. At 24 weeks of age (hypertensive stage), SHRSP showed marked cardiomegaly, mainly due to left ventricular hypertrophy. In such hypertrophic myocardium, focal degeneration of myocardial cells and interstitial fibrosis were observed throughout the left ventricle. Isocitrate dehydrogenase (ICDH), which is related to energy production, was significantly lower in 24-week-old SHRSP myocardium than in WKY. Furthermore, superoxide dismutase (SOD), a potent radical scavenger, was also lower in 24-week-old SHRSP myocardium. On the other hand, RFLP analysis by Rsa I revealed the two deletions in the electrophoresis of fragments in the 24-week-old SHRSP myocardium, but not in the liver. These findings clearly indicate the decrease of mitochondrial function in hypertensive stage showing severe left ventricular hypertrophy. Although the precise mechanisms of such dysfunction were unclear, some of them may be related, at least partly, to mtDNA alteration. Free radical(s) may be a key factor for such mitochondrial changes, because the mitochondria is the major source of free radical generation and SOD activity may be inadequate for elimination of free radical(s) in SHRSP heart.
- 近畿大学の論文
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- Pathophysiological characteristics of mitochondria and structural abnormality of mitochondrial DNA in hypertrophied myocardium of stroke-prone SHR