Reactive Oxygen Radicals in Signaling and Damage in the Ischemic Brain

By P. Chan. Journal of Cerebral Blood Flow and Metabolism, 2001

1,629 citations recorded by the source corpus.

Subfields: Biophysics, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/491f7e0cc1937af47d2bf3d658e81cbdc7fa8200

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Citations in the corpus

The inflammatory response in stroke. (2007, background): “Among all the oxidants in the brain parenchyma after MCAO, superoxide anion is a major one, causing direct injury to ischemic brain or by reacting with NO to generate peroxynitrite (Chan, 2001).”
Neuroprotection for ischemic stroke: past, present and future. (2008, neutral): “…et al., 2004) Other neurotransmitters (MacKenzie et al., 1987; Bonvento et al., 1991; Bozzi et al., 2006) Reactive oxygen radicals, oxidative stress (Chan, 2001; Sugawara et al., 2003; Warner et al., 2004) Lipids, prostanoids, cyclooxygenases, lipoxygenases, phospholipases (Bonventre, 1997;…”
Molecular Mechanisms of Ischemia-Reperfusion Injury in Brain: Pivotal Role of the Mitochondrial Membrane Potential in Reactive Oxygen Species Generation (2012, background): “In fact, during brain ischemia/reperfusion, evidence exists for the three above deleterious events occurring within the mitochondria (see [20, 21].”
Oxidative Stress in Ischemic Brain Damage: Mechanisms of Cell Death and Potential Molecular Targets for Neuroprotection (2011, methodology): “However, using modified enzymes such as liposome-entrapped SOD1 or lecithinized SOD1, which has an increased half-life, the BBB becomes permeable, thus alleviating oxidative stress and reducing brain infarct volume by 50% in rodents subjected to tFCI (9).”
Selective Vulnerability of Late Oligodendrocyte Progenitors to Hypoxia–Ischemia (2002, background): “Because ROS production is a well established sequela of ischemia and reperfusion (Chan, 2001), one target of ROS toxicity in late OL progenitors in vivo may be the mitochondria.”
Exosomes as Drug Delivery Vehicles for Parkinson’s Disease Therapy (2015, background): “It was demonstrated that cells of the immune system, and particularly microglia, release pro-inflammatory cytokines in response to different stress conditions [76] leading to neuronal demise [77].”
Extracellular superoxide dismutase in biology and medicine. (2003, background): “Numerous studies have shown that ROS directly damage cellular macromolecules such as nucleic acids, proteins, and lipids, which contribute to extensive cell death in ischemic tissues [155].”
Mitochondrial dysfunction and oxidative stress in metabolic disorders - A Step towards mitochondria based therapeutic strategies (2016, background): “scavenging capacity of antioxidant enzymes that could lead to altered mitochondrial functions by interacting with mitochondrial and cellular components such as DNA, proteins, and lipids [91,159].”
NAD+/NADH and NADP+/NADPH in Cellular Functions and Cell Death: Regulation and Biological Consequences (2008, positive): “Oxidative stress has been indicated as a key mediator of ischemic brain damage (49, 50), Parkinson’s disease (PD) (24, 308, 321), Alzheimer’s disease (AD) (137, 199, 204, 319, 346) and many other diseases (113).”
Pathophysiology of Cerebral Ischemia and Brain Trauma: Similarities and Differences (2004, background): “Oxidative stress leading to calcium accumulation, mitochondrial dysfunction and the production of reactive oxygen radicals is an important mechanism of cell death following both ischemic (Chan, 2001; Globus et al., 1995b) and traumatic insults (Globus et al.”