Linked Life Data

14757320

Source:http://linkedlifedata.com/resource/pubmed/id/14757320

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-2-3
pubmed:abstractText
Low concentrations of arachidonic acid monoepoxides protect against ischemia/reperfusion injury. This study examined whether low concentrations of the linoleic acid monoepoxide, cis-12,13-epoxy-9-octadecenoic acid (12,13-EOA), protect renal cells against decreases in mitochondrial and transport functions induced by hypoxia/reoxygenation. Primary cultures of rabbit renal proximal tubular cells (RPTC) were pretreated with diluent or 1, 5, or 10 microM 12,13-EOA for 1 h and exposed to 2 h hypoxia/0.5 h reoxygenation in the absence of 12,13-EOA. Basal respiration, oligomycin-sensitive oxygen consumption (QO2), and ATP content decreased 31, 35 and 65%, respectively, following hypoxia/reoxygenation. Hypoxia/reoxygenation also increased mitochondrial membrane potential (DeltaPsi(m)). Pretreatment with 12,13-EOA prevented decreases in basal and oligomycin-sensitive QO2s and increases in DeltaPsi(m). Despite the protection against decreases in mitochondrial function, 12,13-EOA pretreatment did not prevent the initial decrease in intracellular ATP content following hypoxia. However, pretreatment did accelerate the recovery of intracellular ATP levels during reoxygenation. Pretreatment with 12,13-EOA also prevented hypoxia-induced decreases in active Na+ transport. Ouabain-sensitive QO2 (a marker of active Na+ transport) decreased 38% following hypoxia/reoxygenation but was maintained in RPTC pretreated with 1, 5 or 10 microM 12,13-EOA prior to hypoxia. Pretreatment of RPTC with the hydrolyzed product of 12,13-EOA, 12,13-dihydroxyoctadecenoic acid, did not have any protective effects against mitochondrial dysfunction and decreases in active Na+ transport. Thus, this is the first report demonstrating that preconditioning of RPTC with low concentrations of 12,13-EOA, but not its hydrolyzed product, maintains mitochondrial respiration, accelerates restoration of ATP levels, and prevents decreases in active Na+ transport following hypoxia/reoxygenation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0378-4274
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
147
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
161-75
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:14757320-Adenosine Triphosphate, pubmed-meshheading:14757320-Animals, pubmed-meshheading:14757320-Anoxia, pubmed-meshheading:14757320-Biological Transport, Active, pubmed-meshheading:14757320-Cell Hypoxia, pubmed-meshheading:14757320-Cells, Cultured, pubmed-meshheading:14757320-Female, pubmed-meshheading:14757320-Fluorescent Dyes, pubmed-meshheading:14757320-Kidney Tubules, Proximal, pubmed-meshheading:14757320-L-Lactate Dehydrogenase, pubmed-meshheading:14757320-Linoleic Acids, pubmed-meshheading:14757320-Membrane Potentials, pubmed-meshheading:14757320-Mitochondria, pubmed-meshheading:14757320-Oleic Acids, pubmed-meshheading:14757320-Oxygen Consumption, pubmed-meshheading:14757320-Proton-Translocating ATPases, pubmed-meshheading:14757320-Rabbits, pubmed-meshheading:14757320-Sodium
pubmed:year
2004
pubmed:articleTitle
Linoleic acid epoxide promotes the maintenance of mitochondrial function and active Na+ transport following hypoxia.
pubmed:affiliation
Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR 72205-7199, USA. gnowak@uams.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't