Publication Detail
The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Bcl-2 protects neural cells from cyanide/aglycemia-induced lipid oxidation, mitochondrial injury, and loss of viability.
K M Myers; G Fiskum; Y Liu; S J Simmens; D E Bredesen; A N Murphy (Profiled Author: Gary M Fiskum)
Department of Biochemistry and Molecular Biology, George Washington University Medical Center, Washington, DC 20037, USA.
Journal of neurochemistry 1995;65(6):2432-40.
The protooncogene bcl-2 rescues cells from a wide variety of insults. Recent evidence suggests that the mechanism of action of Bcl-2 involves antioxidant activity. The involvement of free radicals in ischemia/reperfusion injury to neural cells has led us to investigate the effect of Bcl-2 in a model of delayed neural cell death. We have examined the survival of control and bcl-2 transfectants of a hypothalamic tumor cell line, GT1-7, exposed to potassium cyanide in the absence of glucose (chemical hypoxia/aglycemia). After 30 min of treatment, no loss of viability was evident in control or bcl-2 transfectants; however, Bcl-2-expressing cells were protected from delayed cell death measured following 24-72 h of reoxygenation. Under these conditions, the rate and extent of ATP depletion in response to treatment with cyanide in the absence of glucose and the rate of recovery of ATP during reenergization were similar in control and Bcl-2-expressing cells. Bcl-2-expressing cells were protected from oxidative damage resulting from this treatment, as indicated by significantly lower levels of oxidized lipids. Mitochondrial respiration in control but not Bcl-2-expressing cells was compromised immediately following hypoxic treatment. These results indicate that Bcl-2 can protect neural cells from delayed death resulting from chemical hypoxia and reenergization, and may do so by an antioxidant mechanism. The results thereby provide evidence that Bcl-2 or a Bcl-2 mimetic has potential therapeutic application in the treatment of neuropathologies involving oxidative stress, including focal and global cerebral ischemia.
1 Originating Grant
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1.
Fiskum, Gary
Molecular Mechanisms of Ischemia Reperfusion Brain Injury
1 May 1995 - 31 December 2008
NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
Scientific Context
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
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1.
2001S S Martin; P Leder
Molecular and cellular biology 2001;21(19):6529-36. -
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2004Brian M Polster; Gary Fiskum
Mitochondrial mechanisms of neural cell apoptosis.
Journal of neurochemistry 2004;90(6):1281-9. -
3.
2005Lucian Soane; Gary Fiskum
Journal of neurochemistry 2005;95(1):230-43.
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