Age-dependent mitochondrial energy dynamics in the mice heart: role of superoxide dismutase-2.
Age-dependent mitochondrial energy dynamics in the mice heart: role of superoxide dismutase-2.
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DOI：
10.1016/j.exger.2013.06.002
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发表时间：
2013-09
影响因子：
3.9
通讯作者：
Muniyappa, Harish
中科院分区：
文献类型：
--
作者：
Das, Kumuda C.;Muniyappa, Harish
关键词：
衰老过程会改变心脏生理机能，减少心肌细胞数量并改变能量代谢。衰老过程中的线粒体功能障碍被认为是导致心脏功能和表型变化的原因。尽管精确了解衰老过程中线粒体呼吸的变化对于管理老年人群的心脏病是必要的，但有关心脏线粒体电子传递链特定复合物功能的相互矛盾的数据限制了干预过程。我们通过线粒体耦合和电子流测定来解决这些问题，以评估从年轻或老年小鼠中分离出的线粒体的特定功能缺陷。我们的结果表明，与年轻小鼠相比，老年小鼠的心脏线粒体通过复合物 I、II 或 IV 利用氧气的速率较低。我们进一步表明，与年轻的野生型小鼠相比，年轻 Sod2+/- 小鼠心脏的线粒体功能下降。然而，与年轻的 Sod2+/- 小鼠心脏相比，老年 Sod2+/- 小鼠心脏的线粒体功能保持不变。此外，老年野生型小鼠和老年 Sod2+/- 小鼠心脏线粒体的耗氧量仍然相似。 Sod2在年轻或年老Sod2+/-小鼠心脏中的表达和活性保持不变。这些数据表明，老年野生型或老年 Sod2+/- 小鼠中氧利用率的降低可能导致线粒体 ROS 介导的氧化损伤减少，需要较少的 Sod2 来保护其免受线粒体氧化应激。
The aging process alters cardiac physiology, decreases the number of cardiomyocytes and alters the energy metabolism. Mitochondrial dysfunction in aging is believed to cause these functional and phenotypic changes in the heart. Although precise understanding of alterations of mitochondrial respiration in aging is necessary to manage heart diseases in the elderly population conflicting data on the function of specific complex of electron transport chain of the heart mitochondria limits the intervention process. We have addressed these issues using the assay of mitochondrial coupling and electron flow to assess specific functional defects in mitochondria isolated from young or aged mice. Our results demonstrate that cardiac mitochondria from older mice utilize oxygen at a decreased rate via complex I, II or IV compared to younger mice. We further show that mitochondrial function decreases in young Sod2+/− mice heart compared to young wildtype mice. However, the mitochondrial function remains unchanged in older Sod2+/− mice heart compared to younger Sod2+/− mice heart. Further, the oxygen consumption remains similar in old wildtype mice and old Sod2+/− mice heart mitochondria. The expression and activity of Sod2 in young or old Sod2+/− mice heart remain unchanged. These data demonstrate that decreased oxygen utilization in older age could have resulted in decreased mitochondrial ROS-mediated oxidative damage requiring less Sod2 for protection against mitochondrial oxidative stress in older wildtype or older Sod2+/− mice.
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