Linked Life Data

20868662

Source:http://linkedlifedata.com/resource/pubmed/id/20868662

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-12-6
pubmed:abstractText
The accumulation of malondialdehyde (MDA), a lipid peroxidation by-product that has been used as an indicator of cellular oxidation status, is significantly increased in many neurological diseases such as brain ischemia/reperfusion, Alzheimer's disease and Parkinson's disease in vivo. In the present study, we found that MDA treatment in vitro reduced cortical neuronal viability in a time- and dose-dependent manner and induced cellular apoptosis as well as necrosis simultaneously. Furthermore, exposure to MDA led to accumulation of intracellular reactive oxygen species, dysfunction of mitochondria (denoted by the loss of mitochondrial transmembrane potential (??m)) and activation of JNK and ERK. Carnosine exhibited better protection against MDA-induced cell injury than antioxidant N-acetyl-cysteine (NAC) with its multi-potency, which alleviated MDA-induced protein cross-linking, ??m decrease, reactive oxygen species burst, JNK and ERK activation. In conclusion, our results suggest that MDA induced cell injury in vitro via protein cross-linking and successive mitochondrial dysfunction, and the activation of reactive oxygen species-dependent MAPK signaling pathway. Carnosine alleviated all these alterations induced by MDA, but NAC merely inhibited Bcl-2 family-related activation of JNK and ERK. These results prompt the possibility that carnosine, but not other conventional antioxidants, can protect neurons against MDA-induced injury through decomposition of protein cross-linking toxicity and may serve as a novel agent in the treatment of neurodegenerative diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1879-0712
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
10
pubmed:volume
650
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
184-94
pubmed:meshHeading
pubmed-meshheading:20868662-Animals, pubmed-meshheading:20868662-Apoptosis, pubmed-meshheading:20868662-Carnosine, pubmed-meshheading:20868662-Cells, Cultured, pubmed-meshheading:20868662-Cerebral Cortex, pubmed-meshheading:20868662-Cross-Linking Reagents, pubmed-meshheading:20868662-Dose-Response Relationship, Drug, pubmed-meshheading:20868662-MAP Kinase Signaling System, pubmed-meshheading:20868662-Malondialdehyde, pubmed-meshheading:20868662-Membrane Potential, Mitochondrial, pubmed-meshheading:20868662-Mitochondria, pubmed-meshheading:20868662-Necrosis, pubmed-meshheading:20868662-Neurons, pubmed-meshheading:20868662-Proteins, pubmed-meshheading:20868662-Rats, pubmed-meshheading:20868662-Rats, Sprague-Dawley, pubmed-meshheading:20868662-Reactive Oxygen Species, pubmed-meshheading:20868662-Time Factors
pubmed:year
2011
pubmed:articleTitle
The cytotoxic mechanism of malondialdehyde and protective effect of carnosine via protein cross-linking/mitochondrial dysfunction/reactive oxygen species/MAPK pathway in neurons.
pubmed:affiliation
Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't