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Journal ArticleDOI

Mitochondrial contributions to tissue damage in stroke.

Neil R. Sims, +1 more
- 01 May 2002 - 
- Vol. 40, Iss: 6, pp 511-526
TLDR
Although evaluating mitochondrial properties in intact brain is difficult, evidence for several potentially deleterious responses to cerebral ischemia or post-ischemic reperfusion have been obtained from investigations using animal models of stroke.
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This article is published in Neurochemistry International.The article was published on 2002-05-01. It has received 316 citations till now. The article focuses on the topics: Reperfusion injury & Mitochondrial permeability transition pore.

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Citations
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Journal ArticleDOI

Nitric Oxide and Peroxynitrite in Health and Disease

TL;DR: Current evidence indicates that most of the cytotoxicity attributed to NO is rather due to peroxynitrite, produced from the diffusion-controlled reaction between NO and another free radical, the superoxide anion, which is presented in detail in this review.
Journal ArticleDOI

Apoptotic Mechanisms After Cerebral Ischemia

TL;DR: Accumulating evidence now indicates that apoptosis is prevalent in nonneuronal cells and that caspase-independent mechanisms also play a key role in the development of apoptosis in ischemic lesions.
Journal Article

Studies on free radicals, antioxidants, and co-factors.

TL;DR: The aim of this review is to highlight the main themes from studies on free radicals, antioxidants and co-factors, and to propose an evidence-based strategy for healthy aging.
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Mitochondrial glutathione, a key survival antioxidant.

TL;DR: From the evaluation ofmGSH influence on different pathologic settings such as hypoxia, ischemia/reperfusion injury, aging, liver diseases, and neurologic disorders, it is becoming evident that it has an important role in the pathophysiology and biomedical strategies aimed to boost mGSH levels.
Journal ArticleDOI

Mitochondria, oxidative metabolism and cell death in stroke

TL;DR: Pharmacological interventions and genetic modifications in rodent models strongly implicate caspase-dependent and caspases-independent apoptosis and the mitochondrial permeability transition as important contributors to tissue damage, particularly when induced by short periods of temporary focal ischemia.
References
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Journal ArticleDOI

The biochemistry of apoptosis

TL;DR: The basic components of the death machinery are reviewed, how they interact to regulate apoptosis in a coordinated manner is described, and the main pathways that are used to activate cell death are discussed.
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Mitochondrial control of cell death

TL;DR: In many instances, permeabilization of mitochondrial membranes is a rate-limiting step of apoptotic or necrotic cell demise, which has important consequences for the pathophysiology of cell death, as well as for its pharmacological control.
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Ischemic Cell Death in Brain Neurons

TL;DR: A major unifying thread of the review is a consideration of how the changes occurring during and after ischemia conspire to produce damaging levels of free radicals and peroxynitrite to activate calpain and other Ca(2+)-driven processes that are damaging, and to initiate the apoptotic process.
Journal ArticleDOI

The mitochondrial permeability transition pore and its role in cell death.

TL;DR: Current evidence that the pore complex is involved in outer-membrane rupture and release of these proteins during programmed cell death is reviewed, along with indications that transient pore opening may provoke 'accidental' apoptosis.
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