The purpose of this review is to integrate available data on the effect of brain ischemia/reperfusion (I/R) on mitochondrial complex I. Complex I is a key component of the mitochondrial respiratory chain and it is the only enzyme responsible for regenerating NAD+ for the maintenance of energy metabolism. The vulnerability of brain complex I to I/R injury has been observed in multiple animal models, but the mechanisms of enzyme damage have not been studied. This review summarizes old and new data on the effect of cerebral I/R on mitochondrial complex I, focusing on a recently discovered mechanism of the enzyme impairment. We found that the loss of the natural cofactor flavin mononucleotide (FMN) by complex I takes place after brain I/R. Reduced FMN dissociates from the enzyme if complex I is maintained under conditions of reverse electron transfer when mitochondria oxidize succinate accumulated during ischemia. The potential role of this process in the development of mitochondrial I/R damage in the brain is discussed.

中文翻译：

---

线粒体复合物I损伤在脑缺血/再灌注损伤中的机制。一个假设。

这篇综述的目的是整合有关脑缺血/再灌注（I / R）对线粒体复合物I的影响的可用数据。复合物I是线粒体呼吸链的关键组成部分，并且是唯一可为NAD +再生的酶。维持能量代谢。在多种动物模型中均已观察到脑复合物I对I / R损伤的脆弱性，但尚未研究酶损伤的机制。这篇综述总结了关于脑I / R对线粒体复合体I的影响的新数据和新数据，重点是最近发现的酶损伤机制。我们发现，复杂的I导致天然辅因子黄素单核苷酸（FMN）的丢失发生在大脑I / R之后。如果线粒体氧化缺血过程中积累的琥珀酸酯时，如果复合物I保持在反向电子转移条件下，则还原的FMN会从酶上解离。讨论了该过程在脑线粒体I / R损伤发展中的潜在作用。