Reactive species mechanisms of cellular hypoxia-reoxygenation injury

Abstract

Li, Chuanyu, and Robert M. Jackson. Reactive species mechanisms of cellular hypoxia-reoxygenation injury. Am J Physiol Cell Physiol 282: C227-C241, 2002; 10.1152/ajpcell.00112.2001.-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 Ϫ ) and release H2O2, 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.anoxia; ischemia; reperfusion BACKGROUND

Cytoglobin, a Novel Member of the Globin Family, Protects Kidney Fibroblasts against Oxidative Stress under Ischemic Conditions

“…4 On this basis, up-regulation of Cygb in the hypoxic kidney may be an adaptive response to increase the efficiency of mitochondrial respiration under oxygen deprivation states. In addition, oxidative stress likely mediates many of the deleterious effects of I/R injury, 36,37 with the tubulointerstitium as the main target. 38,39 Recent studies suggest that Cygb may sense oxygen concentration and act as a regulatory protein that protects cells from ROS.…”

The protective effects of curcumin on intestine and remote organs against mesenteric ischemia/reperfusion injury

“…The critical ischemic period is dependent on the organ, and is about 15-20 minutes (min) in the liver and kidney (2). Reperfusion of the superior mesenteric artery (SMA) causes activation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), and a large amount of nitric oxide, proinflammatory and inflammatory cytokines and transcription factors are activated after mesenteric I/R injury and circulate via both the venous and lymphatic system, inducing remote organ injury (3,4) including the lungs, kidneys and liver (4,5). ROS formation results in injury via various biomolecules found in tissues, including membrane lipids, nucleic acids, enzymes, and receptors.…”

Alterations in Carotid Body Morphology and Cellular Mechanism Under the Influence of Intermittent Hypoxia

“…As discussed earlier, OSA disrupts equilibrium between HIF1α and HIF2α resulting in imbalance between NOX2 and SOD2 respectively [16] that leads to ROS formation [14,15]. This leads to DNA damage, depletion of intracellular antioxidant defense system, alteration in calcium homeostasis and apoptosis [30] and further causes pathophysiology. On the contrary, the oxidant-antioxidant homeostasis, leading to low levels of ROS production may serve as messengers in order to activate signaling pathways and is also involved in O 2 sensing that influences HIF stability [31].…”