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Reactive species mechanisms of cellular hypoxia-reoxygenation injury

Li, Chuanyu, Jackson, Robert M.·2002·American Journal of Physiology-Cell Physiology

Abstract

Exacerbation of hypoxic injury after restoration of oxygenation (reoxygenation) is an important mechanism of cellular injury in transplantation and in myocardial, hepatic, intestinal, cerebral, renal, and other ischemic syndromes. Cellular hypoxia and reoxygenation are two essential elements of ischemia-reperfusion injury. Activated neutrophils contribute to vascular reperfusion injury, yet posthypoxic cellular injury occurs in the absence of inflammatory cells through mechanisms involving reactive oxygen (ROS) or nitrogen species (RNS). Xanthine oxidase (XO) produces ROS in some reoxygenated cells, but other intracellular sources of ROS are abundant, and XO is not required for reoxygenation injury. Hypoxic or reoxygenated mitochondria may produce excess superoxide (O[Formula: see text]) and release H 2 O 2, a diffusible long-lived oxidant that can activate signaling pathways or react vicinally with proteins and lipid membranes. This review focuses on the specific roles of ROS and RNS in the cellular response to hypoxia and subsequent cytolytic injury during reoxygenation.

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Metadata

Authors
Li, C., & Jackson, R. M.
Venue
American Journal of Physiology-Cell Physiology
Published
2002-02-01
Volume
282
Issue
2
Pages
C227-C241
ISSN
  • 0363-6143 (ISSN-L)
  • 1522-1563
OpenAlex
W2150951327
Cited by
1,043
References
10
FWCI
16.74
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Reactive species mechanisms of cellular hypoxia-reoxygenation injury. https://app.cochat.ai/papers/10.1152/ajpcell.00112.2001
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Li, C., & Jackson, R. M. (2002). Reactive species mechanisms of cellular hypoxia-reoxygenation injury. American Journal of Physiology-Cell Physiology. https://doi.org/10.1152/ajpcell.00112.2001

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