Interaction between free radicals and zinc following cerebral ischemia/reperfusion injury

doi:10.3969/j.issn.1006-7795.2018.03.012

Abstract

Abstract: Cerebral ischemia/reperfusion induces the production of a large amount of free radicals, triggers oxidative stress, and results in the accumulation of intracellular zinc (Zn²⁺) in various ways. It is reported that the intracellular Zn²⁺ release and the generation of reactive oxygen species (ROS) are common ingredients in numerous toxic signaling mechanisms in neurons. Both Zn²⁺ ROS have been shown to accumulate during hypoxic-ischemic stress and play important roles in pathological processes. Liberated Zn²⁺ induces ROS generation by multiple mechanisms, including not only the induction of mitochondrial ROS production, and also the promotion of ROS formation outside the mitochondria by other routes such as interaction with NADPH oxidase. The interaction between Zn²⁺ and ROS eventually contributes to neuronal damage via apoptotic pathways or signal transduction. However, under certain conditions, Zn²⁺ has antioxidant activity and protects brain from injury. In this paper, the interaction between free radicals and Zn²⁺ following cerebral ischemia/reperfusion injury are reviewed.

Key words: Zn²⁺, free radicals, oxidative stress, reactive oxygen species, cerebral ischemia

CLC Number:

R743.3

Fang Yalan, Yin Jie, Liu Kejian, Zhao Yongmei. Interaction between free radicals and zinc following cerebral ischemia/reperfusion injury[J]. Journal of Capital Medical University, 2018, 39(3): 373-377.

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URL: https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/10.3969/j.issn.1006-7795.2018.03.012

https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/Y2018/V39/I3/373

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