Cardiac complex II activity is enhanced by fat and mediates greater mitochondrial oxygen consumption following hypoxic re-oxygenation
Cardiac complex II activity is enhanced by fat and mediates greater mitochondrial oxygen consumption following hypoxic re-oxygenation
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脂肪增强心脏复合物 II 的活性，并在缺氧复氧后介导更大的线粒体耗氧量
DOI：
10.1007/s00424-020-02355-8
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发表时间：
2020-02-20
影响因子：
4.5
通讯作者：
Zhang, Yin Hua
中科院分区：
文献类型：
--
作者：
Zhu, Shi Chao;Chen, Chen;Zhang, Yin Hua
最近的证据表明，线粒体复合物II是心肌缺血再灌注损伤的重要介质。本研究旨在探讨补充脂肪酸或高脂饮食（HFD）对心肌线粒体活性的影响。在此条件下，研究了缺氧和复氧后复合物I和复合物II活性以及线粒体耗氧率（OCR）的变化。我们的研究结果表明，OCR（线粒体活性）与棕榈酰肉毒碱补充C57 BL/6小鼠心脏中的富含维生素A的部分显着增加。线粒体复合物I活性不受棕榈酰肉碱的影响，但复合物II活性增强。缺氧30分钟后再充氧短暂增加OCR，但这种对OCR的影响被取消复合物II抑制剂，丙二酸，但不是由复合物I抑制剂，鱼藤酮，尽管复合物I的活性显着增加与缺氧后在棕榈酰肉毒碱的存在下再充氧。此外，OCR和复合物II活性显着增加线粒体从高脂饮食小鼠心脏相比，正常或低脂饮食小鼠。缺氧30分钟后，线粒体再充氧增加了所有三组的OCR，但在HFD中显着更多。丙二酸盐在所有组中消除了再氧合诱导的OCR增加。我们的研究结果表明，复合物II的活性和OCR增强与棕榈酰肉碱或在HFD小鼠心脏。虽然缺氧后复氧增强复合物II和复合物I的活动，复合物II起着重要的作用，增加线粒体活性，这可能是有助于心肌缺血再灌注损伤。
Recent evidence suggests that mitochondrial complex II is an essential mediator of myocardial ischemia-reperfusion injury. The present study aimed to investigate the effects of fatty acid supplementation or high-fat diet (HFD) on cardiac mitochondrial activity. The changes of complex I and complex II activities and mitochondrial oxygen consumption rate (OCR) following hypoxia and re-oxygenation under these conditions were studied. Our results have shown that OCR (mitochondrial activity) was significantly increased with palmitoylcarnitine supplementation in mitochondria-enriched fraction from C57BL/6 mice hearts. Mitochondrial complex I activity was unaffected by palmitoylcarnitine but complex II activity was enhanced. Re-oxygenation following 30-min hypoxia transiently increased OCR but such an effect on OCR was abolished by complex II inhibitor, malonate, but not by complex I inhibitor, rotenone, despite that complex I activity was significantly increased with re-oxygenation following hypoxia in the presence of palmitoylcarnitine. Furthermore, OCR and complex II activity were significantly increased in the mitochondria from high-fat diet mice heart compared with those of normal or low-fat diet mice. Re-oxygenation to mitochondria following 30-min hypoxia increased OCR in all three groups but significantly more in HFD. Malonate abolished re-oxygenation-induced OCR increment in all groups. Our results indicate that complex II activity and OCR are enhanced with palmitoylcarnitine or in HFD mice heart. Although re-oxygenation following hypoxia enhanced complex II and complex I activities, complex II plays an important role in increasing mitochondrial activity, which may be instrumental in myocardial injury following ischemic reperfusion.