This review focuses on the problem of oxidative stress in early brain injury (EBI) after spontaneous subarachnoid hemorrhage (SAH). EBI involves complex pathophysiological mechanisms, including oxidative stress. In the first section, we describe the main sources of free radicals in EBI. There are several sources of excessive generation of free radicals from mitochondrial free radicals’ generation and endoplasmic reticulum stress, to hemoglobin and enzymatic free radicals’ generation. The second part focuses on the disruption of antioxidant mechanisms in EBI. The third section describes some newly found molecular mechanisms and pathway involved in oxidative stress after EBI. The last section is dedicated to the pathophysiological mechanisms through which free radicals mediate early brain injury.

中文翻译：

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氧化应激在蛛网膜下腔出血后早期脑损伤中的作用

这篇综述的重点是自发性蛛网膜下腔出血（SAH）后早期脑损伤（EBI）的氧化应激问题。EBI涉及复杂的病理生理机制，包括氧化应激。在第一部分中，我们描述了EBI中自由基的主要来源。从线粒体自由基的产生和内质网应激到血红蛋白和酶促自由基的产生，自由基的过量产生有多种来源。第二部分着眼于EBI中抗氧化机制的破坏。第三部分描述了一些新发现的分子机制和途径，涉及EBI后的氧化应激。最后一部分专门讨论自由基介导早期脑损伤的病理生理机制。