Document Detail

Arachidonic acid and leukotriene C4: role in transient cerebral ischemia of gerbils.
MedLine Citation:
PMID:  10492517     Owner:  NLM     Status:  MEDLINE    
Accumulation of arachidonic acid (AA) is greatest in brain regions most sensitive to transient ischemia. Free AA released after ischemia is either: 1) reincorporated into the membrane phospholipids, or 2) oxidized during reperfusion by lipoxygenases and cyclooxygenases, producing leukotrienes (LT), prostaglandins, thromboxanes and oxygen radicals. AA, its metabolite LTC4 and lipid peroxides (generated during AA metabolism) have been implicated in the blood-brain barrier (BBB) dysfunction, edema and neuronal death after ischemia/reperfusion. This report describes the time course of AA release, LTC4 accumulation and association with the physiological outcome during transient cerebral ischemia of gerbils. Significant amount of AA was detected immediately after 10 min ischemia (0 min reperfusion) which returned to sham levels within 30 min reperfusion. A later release of AA occurred after 1 d. LTC4 levels were elevated at 0-6 h and 1 d after ischemia. Increased lipid peroxidation due to AA metabolism was observed between 2-6 h. BBB dysfunction occurred at 6 h. Significant edema developed at 1 and 2 d after ischemia and reached maximum at 3 d. Ischemia resulted in approximately 80% neuronal death in the CA1 hippocampal region. Pretreatment with a 5-lipoxygenase inhibitor, AA861 resulted in significant attenuation of LTC4 levels (Baskaya et al. 1996. J. Neurosurg. 85: 112-116) and CA1 neuronal death. Accumulation of AA and LTC4, together with highly reactive oxygen radicals and lipid peroxides, may alter membrane permeability, resulting in BBB dysfunction, edema and ultimately to neuronal death.
A M Rao; J F Hatcher; M S Kindy; R J Dempsey
Related Documents :
25256737 - Development of the knee oa pre-screening questionnaire.
25435767 - Construct and concurrent validation of a new resistance intensity scale for exercise wi...
10492517 - Arachidonic acid and leukotriene c4: role in transient cerebral ischemia of gerbils.
9220357 - Intermittent ischemia: energy metabolism, cellular volume regulation, adenosine and ins...
7105377 - Exercise effect upon plasma melatonin levels in women: possible physiological significa...
1855267 - Exercise participation after menopause.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Neurochemical research     Volume:  24     ISSN:  0364-3190     ISO Abbreviation:  Neurochem. Res.     Publication Date:  1999 Oct 
Date Detail:
Created Date:  1999-10-18     Completed Date:  1999-10-18     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7613461     Medline TA:  Neurochem Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1225-32     Citation Subset:  IM    
Department of Neurological Surgery, University of Wisconsin, Madison 53792-3232, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Arachidonic Acid / physiology*
Blood-Brain Barrier
Brain Edema / metabolism,  pathology
Ischemic Attack, Transient / metabolism,  pathology,  physiopathology*
Leukotriene C4 / physiology*
Lipid Peroxidation
Grant Support
Reg. No./Substance:
506-32-1/Arachidonic Acid; 72025-60-6/Leukotriene C4

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Striatum adenosine A2 receptors are modified during seizure: effect of cyclopentyladenosine administ...
Next Document:  In-vitro and in-vivo action of cannabinoids.