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首页> 外文期刊>Molecular and Cellular Biology >Cells Lacking Rieske Iron-Sulfur Protein Have a Reactive Oxygen Species-Associated Decrease in Respiratory Complexes I and IV
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Cells Lacking Rieske Iron-Sulfur Protein Have a Reactive Oxygen Species-Associated Decrease in Respiratory Complexes I and IV

机译：缺乏里斯克铁硫蛋白的细胞在呼吸复合物I和IV中具有活性氧相关的减少

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摘要

Mitochondrial respiratory complexes of the electron transport chain (CI, CIII, and CIV) can be assembled into larger structures forming supercomplexes. We analyzed the assembly/stability of respiratory complexes in mouse lung fibroblasts lacking the Rieske iron-sulfur protein (RISP knockout [KO]cells), one of the catalytic subunits of CIII. In the absence of RISP, most of the remaining CIII subunits were able to assemble into a large precomplex that lacked enzymatic activity. CI, CIV, and supercomplexes were decreased in the RISP-deficient cells. Reintroduction of RISP into KO cells restored CIII activity and increased the levels of active CI, CIV, and supercomplexes. We found that hypoxia (1% O2) resulted in increased levels of CI, CIV, and supercomplex assembly in RISP KO cells. In addition, treatment of control cells with different oxidative phosphorylation (OXPHOS) inhibitors showed that compounds known to generate reactive oxygen species (ROS) (e.g., antimycin A and oligomycin) had a negative impact on CI and supercomplex levels. Accordingly, a superoxide dismutase (SOD) mimetic compound and SOD2 overexpression provided a partial increase in supercomplex levels in the RISP KO cells. Our data suggest that the stability of CI, CIV, and supercomplexes is regulated by ROS in the context of defective oxidative phosphorylation.
机译：电子传输链的线粒体呼吸复合物（CI，CIII和CIV）可以组装成更大的结构，形成超复合物。我们分析了缺少Rieske铁-硫蛋白（RISP敲除[KO]细胞）（CIII的催化亚基之一）的小鼠肺成纤维细胞中呼吸复合物的装配/稳定性。在没有RISP的情况下，大多数剩余的CIII亚基都能够组装成缺乏酶促活性的大型预复合物。 CI，CIV和超复合物在RISP缺陷细胞中降低。将RISP重新引入KO细胞可恢复CIII活性并增加活性CI，CIV和超复合物的水平。我们发现缺氧（1％O 2 ）导致RISP KO细胞中CI，CIV和超复杂装配的水平增加。此外，用不同的氧化磷酸化（OXPHOS）抑制剂处理对照细胞表明，已知会产生活性氧（ROS）的化合物（例如，抗霉素A和寡聚霉素）对CI和超配合物水平有负面影响。因此，超氧化物歧化酶（SOD）模拟化合物和SOD2过表达使RISP KO细胞中的超复合物水平部分升高。我们的数据表明，在有缺陷的氧化磷酸化的情况下，ROS可以调节CI，CIV和超配合物的稳定性。

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