Reactive species mechanisms of cellular hypoxia-reoxygenation injury

Chuanyu Li, Robert M. Jackson

Research output: Contribution to journalReview articlepeer-review

873 Scopus citations


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 2 -) and release H 2O 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.

Original languageEnglish (US)
Pages (from-to)C227-C241
JournalAmerican Journal of Physiology - Cell Physiology
Issue number2 51-2
StatePublished - 2002
Externally publishedYes


  • Anoxia
  • Ischemia
  • Reperfusion

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology


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