Moghaddas Shadi, Stoll Maria S K, Minkler Paul E, Salomon Robert G, Hoppel Charles L, Lesnefsky Edward J
Department of Medicine, Divisions of Cardiology, Case Western Reserve University, Cleveland, Ohio, USA.
J Gerontol A Biol Sci Med Sci. 2002 Jan;57(1):B22-8. doi: 10.1093/gerona/57.1.b22.
Aging selectively decreases the rate of oxidative phosphorylation in the interfibrillar population of cardiac mitochondria (IFM) located between the myofibers. In contrast, subsarcolemmal mitochondria (SSM), located below the plasma membrane, remain unaffected. IFM from elderly (24-month-old) Fischer 344 rats have a decreased specific activity of complexes III and IV. Complexes III and IV require an inner mitochondrial membrane lipid environment enriched in the oxidatively sensitive phospholipid cardiolipin for maximal activity. We asked if aging decreases the content or alters the composition of cardiolipin as a potential mechanism of the aging defect in IFM. The content and composition of mitochondrial phospholipids were measured in SSM and IFM from adult and aging rat hearts. Aging did not alter the content of mitochondrial phospholipids, including cardiolipin, in either population of mitochondria. The composition of cardiolipin based on characterization of both acyl group and the individual molecular species of cardiolipin was also unaltered by aging. Lipid-mediated oxidative modification of complex III subunits was not detected, making cardiolipin-derived oxidative damage to complex III unlikely. Thus, alterations in cardiolipin are not the mechanism for the aging defect in IFM in Fischer 344 rats.
衰老选择性地降低了位于心肌纤维之间的肌原纤维间心脏线粒体群体（IFM）中的氧化磷酸化速率。相比之下，位于质膜下方的肌膜下线粒体（SSM）则不受影响。老年（24月龄）Fischer 344大鼠的IFM中复合物III和IV的比活性降低。复合物III和IV需要富含氧化敏感磷脂心磷脂的线粒体内膜脂质环境才能发挥最大活性。我们研究衰老是否会降低心磷脂的含量或改变其组成，以此作为IFM衰老缺陷的潜在机制。我们测定了成年和老龄大鼠心脏中SSM和IFM中线粒体磷脂的含量和组成。衰老并未改变这两种线粒体群体中线粒体磷脂（包括心磷脂）的含量。基于心磷脂酰基和单个分子种类特征的心磷脂组成也未因衰老而改变。未检测到复合物III亚基的脂质介导氧化修饰，因此心磷脂衍生的复合物III氧化损伤不太可能发生。因此，心磷脂的改变不是Fischer 344大鼠IFM衰老缺陷的机制。
