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马属动物疾病中的氧化损伤机制。

Mechanisms of oxidative injury in equine disease.

作者信息

Wong David M, Moore Rustin M, Brockus Charles W

机构信息

Iowa State University, Ames, IA, USA.

出版信息

Compend Contin Educ Vet. 2012 Aug;34(8):E6.

PMID:22935994
Abstract

Oxygen is essential to aerobic life, but it is also associated with the production of highly reactive compounds that can pose danger to physiologic systems when the oxygen concentration is excessive. Reactive oxygen species (ROS) are required for normal physiologic processes, but when produced in excess, they can overwhelm endogenous antioxidants, resulting in significant cellular damage and, eventually, cell death. Ischemic events can initiate numerous pathophysiologic mechanisms leading to increased production of ROS, loss of cellular energy production, and lipid peroxidation. Although reperfusion is a necessary step in cellular recovery from ischemia, it can be deleterious by leading to the generation of even more ROS and stimulating the accumulation of neutrophils. Both of these processes may contribute to irreversible cell death and, ultimately, organ failure. This article reviews oxygen metabolism, ischemia, and reperfusion injury and how these processes may occur in equine disorders.

摘要

氧气对于需氧生命至关重要,但它也与高反应性化合物的产生有关,当氧气浓度过高时,这些化合物会对生理系统构成危险。活性氧(ROS)是正常生理过程所必需的,但当产生过量时,它们会超过内源性抗氧化剂的能力,导致显著的细胞损伤,并最终导致细胞死亡。缺血事件可引发众多病理生理机制,导致ROS产生增加、细胞能量产生丧失和脂质过氧化。尽管再灌注是细胞从缺血中恢复的必要步骤,但它可能是有害的,因为它会导致产生更多的ROS并刺激中性粒细胞的积聚。这两个过程都可能导致不可逆的细胞死亡,并最终导致器官衰竭。本文综述了氧代谢、缺血和再灌注损伤,以及这些过程在马属动物疾病中可能如何发生。

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