Reactive oxygen species (ROS) are known participants in several cellular processes. Superoxide anion radical, one example of ROS, forms as a result of normal cellular respiration and is usually cleared successfully by superoxide dismutase (SOD) and other radical scavengers. However, when superoxide exceeds the clearance capacity of SOD and other ROS scavengers, superoxide initiates a number of pathologic processes. This review examines pathologies involving superoxide, including: cancer, neurodegenerative diseases, ischemia/reperfusion injury, and inflammation. We will also explore the basic science principles of superoxide and SOD, including: SOD evolution, SOD mutations, biochemistry, physiology, and pathophysiology. In reviewing the basic science, clinical pathology, and therapeutic research, we hope to clearly demonstrate plausible pharmacologic targets of action. We have revised data about basic science, clinical pathology and therapeutic research in an effort to propose plausible pharmacological targets of action. The understanding of these aspects is critical in the accomplishment of a successful clinical intervention.

中文翻译：

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超氧化物歧化酶：生理药理学更新。

活性氧 (ROS) 是几种细胞过程的已知参与者。超氧阴离子自由基是 ROS 的一个例子，它是正常细胞呼吸的结果，通常被超氧化物歧化酶 (SOD) 和其他自由基清除剂成功清除。然而，当超氧化物超过 SOD 和其他 ROS 清除剂的清除能力时，超氧化物会引发许多病理过程。本综述研究了涉及超氧化物的病理，包括：癌症、神经退行性疾病、缺血/再灌注损伤和炎症。我们还将探索超氧化物和 SOD 的基本科学原理，包括：SOD 进化、SOD 突变、生物化学、生理学和病理生理学。在回顾基础科学、临床病理学和治疗研究时，我们希望清楚地证明合理的药理作用靶点。我们修改了有关基础科学、临床病理学和治疗研究的数据，以提出合理的药理学作用靶点。对这些方面的理解对于成功进行临床干预至关重要。