Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2005-10-21
pubmed:abstractText
Docosahexaenoic acid (DHA, 22:6 n-3) from fish oil, and butyrate, a fiber fermentation product, work coordinately to protect against colon tumorigenesis in part by inducing apoptosis. We have recently demonstrated that dietary DHA is incorporated into mitochondrial membrane phospholipids, thereby enhancing oxidative stress induced by butyrate metabolism. In order to elucidate the subcellular origin of oxidation induced by DHA and butyrate, immortalized young adult mouse colonocytes were treated with 0-200 microM DHA or linoleic acid (LA, 18:2 n-6; control) for 72 h with or without 5 mM butyrate for the final 24 h. Cytosolic reactive oxygen species, membrane lipid oxidation, and mitochondrial membrane potential (MP), were measured by live-cell fluorescence microscopy. After 24 h of butyrate treatment, DHA primed cells exhibited a 151% increase in lipid oxidation (P < 0.01), compared with no butyrate treatment, which could be blocked by a mitochondria-specific antioxidant, 10-(6'-ubiquinoyl) decyltriphenylphosphonium bromide (MitoQ) (P < 0.05). Butyrate treatment of LA pretreated cells did not show any significant effect. In the absence of butyrate, DHA treatment, compared with LA, increased resting MP by 120% (P < 0.01). In addition, butyrate-induced mitochondrial membrane potential (MP), dissipation was 21% greater in DHA primed cells as compared with LA at 6 h. This effect was reversed by preincubation with inhibitors of the mitochondrial permeability transition pore, cyclosporin A or bongkrekic acid (1 microM). The functional importance of these events is supported by the demonstration that DHA and butyrate-induced apoptosis is blocked by MitoQ. These data indicate that DHA and butyrate potentiate mitochondrial lipid oxidation and the dissipation of MP which contribute to the induction of apoptosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0143-3334
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1914-21
pubmed:dateRevised
2011-9-22
pubmed:meshHeading
pubmed-meshheading:15975958-Animals, pubmed-meshheading:15975958-Anti-Bacterial Agents, pubmed-meshheading:15975958-Antioxidants, pubmed-meshheading:15975958-Apoptosis, pubmed-meshheading:15975958-Bongkrekic Acid, pubmed-meshheading:15975958-Butyrates, pubmed-meshheading:15975958-Cells, Cultured, pubmed-meshheading:15975958-Colon, pubmed-meshheading:15975958-Cyclosporine, pubmed-meshheading:15975958-Docosahexaenoic Acids, pubmed-meshheading:15975958-Epithelial Cells, pubmed-meshheading:15975958-Immunosuppressive Agents, pubmed-meshheading:15975958-Linoleic Acid, pubmed-meshheading:15975958-Lipid Peroxidation, pubmed-meshheading:15975958-Membrane Potentials, pubmed-meshheading:15975958-Mice, pubmed-meshheading:15975958-Microscopy, Fluorescence, pubmed-meshheading:15975958-Mitochondria, pubmed-meshheading:15975958-Organophosphorus Compounds, pubmed-meshheading:15975958-Oxidative Stress, pubmed-meshheading:15975958-Ubiquinone
pubmed:year
2005
pubmed:articleTitle
The role of docosahexaenoic acid in mediating mitochondrial membrane lipid oxidation and apoptosis in colonocytes.
pubmed:affiliation
Faculty of Nutrition, Texas A&M University, College Station, TX 77843, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, N.I.H., Extramural