Increased expression of the F1F0 ATP synthase in response to iron in heart mitochondria
Increased expression of the F1F0 ATP synthase in response to iron in heart mitochondria
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DOI：
10.5483/bmbrep.2008.41.2.153
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发表时间：
2008-02-29
期刊：
影响因子：
3.8
通讯作者：
Song, Eunsook
中科院分区：
文献类型：
--
作者：
Kim, Misun;Kim, Jinsun;Song, Eunsook
本研究的目的是确定与铁对大鼠心脏造成的损伤相关的线粒体成分。通过血清中乳酸脱氢酶（LDH）的增加来评估细胞活力的降低。为了评估线粒体的功能完整性，在心脏中测量活性氧（ROS）、呼吸控制比（RCR）、ATP和可螯合铁含量。线粒体中可螯合铁增加了15倍，ROS增加了59%。铁存在下线粒体功能的恶化表现为低RCR（降低46%）和低ATP含量（降低96%）。使用二维凝胶电泳（2DE），我们确定了21个线粒体蛋白质的铁超载触发的变化。值得注意的是，F1F0 ATP合酶的a、β和d亚基的表达随着ATP的丧失而沿着增加。这表明F1F0 ATP合成酶参与铁代谢。
The objective of the present study was to identify mitochondrial components associated with the damage caused by iron to the rat heart. Decreased cell viability was assessed by increased presence of lactate dehydrogenase (LDH) in serum. To assess the functional integrity of mitochondria, Reactive Oxygen Species (ROS), the Respiratory Control Ratio (RCR), ATP and chelatable iron content were measured in the heart. Chelatable iron increased 15-fold in the mitochondria and ROS increased by 59%. Deterioration of mitochondrial function in the presence of iron was demonstrated by low RCR (46% decrease) and low ATP content (96% decrease). Using two dimensional gel electrophoresis (2DE), we identified alterations in 21 mitochondrial proteins triggered by iron overload. Significantly, expression of the a, beta, and d subunits of F1F0 ATP synthase increased along with the loss of ATP. This suggests that the F1F0 ATP synthase participates in iron metabolism.