1
40
2
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2013.02.018" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2013.02.018</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
211-222
Volume
60
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Dublin Core
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Title
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Robust protein nitration contributes to acetaminophen-induced mitochondrial dysfunction and acute liver injury
Publisher
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Free Radical Biology and Medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-07
Subject
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3-Nitrotyrosine; Acetaminophen; Acute liver injury; Biochemistry & Molecular Biology; covalent binding; CYP2E1; Endocrinology & Metabolism; Free radicals; immunohistochemical localization; induced hepatotoxicity; knockout mice; Mitochondrial dysfunction; mouse-liver; n-acetylcysteine; n-acetylcysteine; nitration; nitric-oxide synthase; oxidative stress; protein; superoxide-dismutase; terminal kinase
Creator
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Abdelmegeed M A; Jang S; Banerjee A; Hardwick J P; Song B J
Description
An account of the resource
Acetaminophen (APAP), a widely used analgesic/antipyretic agent, can cause liver injury through increased nitrative stress, leading to protein nitration. However, the identities of nitrated proteins and their roles in hepatotoxicity are poorly understood. Thus, we aimed at studying the mechanism of APAP-induced hepatotoxicity by systematic identification and characterization of nitrated proteins in the absence or presence of an antioxidant, N-acetylcysteine (NAC). The levels of nitrated proteins markedly increased at 2 h in mice exposed to a single APAP dose (350 mg/kg ip), which caused severe liver necrosis at 24 h. Protein nitration and liver necrosis were minimal in mice exposed to nontoxic 3-hydroxyacetanilide or animals co-treated with APAP and NAC. Mass-spectral analysis of the affinity-purified nitrated proteins identified numerous mitochondrial and cytosolic proteins, including mitochondrial aldehyde dehydrogenase, Mn-superoxide dismutase, glutathione peroxidase, ATP synthase, and 3-ketoacyl-CoA thiolase, involved in antioxidant defense, energy supply, or fatty acid metabolism. Immunoprecipitation followed by immunoblot with anti-3-nitrotyrosine antibody confirmed that the aforementioned proteins were nitrated in APAP-exposed mice but not in NAC-cotreated mice. Consistently, NAC cotreatment significantly restored the suppressed activity of these enzymes. Thus, we demonstrate a new mechanism by which many nitrated proteins with concomitantly suppressed activity promotes APAP-induced mitochondrial dysfunction and hepatotoxicity. Published by Elsevier Inc.
Identifier
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<a href="http://doi.org/10.1016/j.freeradbiomed.2013.02.018" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2013.02.018</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2013
3-Nitrotyrosine
Abdelmegeed M A
ACETAMINOPHEN
Acute liver injury
Banerjee A
Biochemistry & Molecular Biology
covalent binding
CYP2E1
Endocrinology & Metabolism
Free Radical Biology and Medicine
Free radicals
Hardwick J P
immunohistochemical localization
induced hepatotoxicity
Jang S
Journal Article or Conference Abstract Publication
knockout mice
Mitochondrial dysfunction
mouse-liver
n-acetylcysteine
nitration
nitric-oxide synthase
Oxidative Stress
Protein
Song B J
superoxide-dismutase
terminal kinase
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/hipo.20048" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hipo.20048</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
246-253
Issue
2
Volume
15
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
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Title
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BDNF protects against stress-induced impairments in spatial learning and memory and UP
Publisher
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Hippocampus
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
2005
Subject
The topic of the resource
adult-rat; brain; central-nervous-system; hippocampal pyramidal neurons; hippocampus; in-vivo; knockout mice; long-term potentiation; neuroprotection; Neurosciences & Neurology; neurotrophic factor; neurotrophins; rat; synaptic plasticity; synaptic transmission
Creator
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Radecki D T; Brown L M; Martinez J; Teyler T J
Description
An account of the resource
The present study investigated whether infusion of brain-derived neurotrophic factor (BDNF) could ameliorate stress-induced impairments in spatial learning and memory as well as hippocampal long-term potentiation (LTP) of rats. Chronic immobilization stress (2 h/day X 7 days) significantly impaired spatial performance in the Morris water maze, elevated plasma corticosterone, and attenuated LTP in hippocampal slices from these animals as compared with normal control subjects. BDNF was infused into the left hippocampus (0.5 mu l/h) for 14 days, beginning 7 days before the stress exposure. The BDNF group was protected from the deleterious effects of stress and performed at a level indistinguishable from normal control animals despite the presence of elevated corticosterone. BDNF alone and sham infusions had no effect on performance or LTP. These results demonstrate that spatial learning and memory, and LTP, a candidate neural substrate of learning and memory, are compromised during chronic stress, and may be protected by BDNF administration. (c) 2004 Wiley-Liss, Inc.
Identifier
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<a href="http://doi.org/10.1002/hipo.20048" target="_blank" rel="noreferrer noopener">10.1002/hipo.20048</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2005
adult-rat
Brain
Brown L M
central-nervous-system
hippocampal pyramidal neurons
Hippocampus
in-vivo
Journal Article
knockout mice
Long-Term Potentiation
Martinez J
Neuroprotection
Neurosciences & Neurology
neurotrophic factor
neurotrophins
Radecki D T
rat
synaptic plasticity
Synaptic Transmission
Teyler T J