Document Detail

Reactive oxygen species play an important role in iodoacetate-induced neurotoxicity in primary rat neuronal cultures and in differentiated PC12 cells.
MedLine Citation:
PMID:  14623125     Owner:  NLM     Status:  MEDLINE    
The role of reactive oxygen species in the pathogenesis of the neurotoxicity associated with ischemia-reperfusion, was investigated in a model of primary rat neuronal cultures and of differentiated PC12 cells, subjected to chemical ischemia by iodoacetic acid (IAA, 2.5 h) followed by a short period of reperfusion (1 h). The injury to the cells was assessed by lactate dehydrogenase (LDH) release into the culture media. The PC12 cells exhibited relative resistance to IAA cytotoxicity. Therefore these cells were studied at a 4-fold higher IAA concentration (400 microM instead of 100 microM for the neurons). The injury to both cell types was significantly greater in the short post-insult reperfusion (PIR) period than during the insult period. The presence, during the combined insult and PIR periods, of alpha-tocopherol (100 microM), melatonin (1 mM) and LY231617 (5 microM), conferred to both cell types considerable protection against the injury occurring during the insult and during the PIR periods (assessed separately). Superoxide dismutase (SOD; 500 IU/ml) conferred protection to the neurons, but not to the PC12 cells. When exposure to the antioxidants was limited to the short (15 min) pre insult period, only LY231617 conferred protection. In the neurons the protection occurred only during the insult period, whereas in the PC12 cells during both the insult and PIR periods. When the exposure to the antioxidants was limited to the PIR period, only SOD conferred protection and only in the neuronal cultures. These findings suggest that neuronal damage caused during ischemia-reperfusion can be diminished markedly by co-presence of antioxidants during the insult period. Certain antioxidants may protect the neurons even when present only before or after the insult.
Oded Sperling; Yael Bromberg; Harrietta Oelsner; Esther Zoref-Shani
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Neuroscience letters     Volume:  351     ISSN:  0304-3940     ISO Abbreviation:  Neurosci. Lett.     Publication Date:  2003 Nov 
Date Detail:
Created Date:  2003-11-19     Completed Date:  2004-01-12     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7600130     Medline TA:  Neurosci Lett     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  137-40     Citation Subset:  IM    
Department of Clinical Biochemistry, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
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MeSH Terms
Antioxidants / pharmacology
Cell Differentiation / drug effects,  physiology
Cells, Cultured
Iodoacetates / toxicity*
Neurons / drug effects*,  metabolism,  pathology
PC12 Cells
Reactive Oxygen Species / metabolism*,  pharmacology
Reperfusion Injury / chemically induced,  metabolism,  pathology
Reg. No./Substance:
0/Antioxidants; 0/Iodoacetates; 0/Reactive Oxygen Species

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