Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-10-26
pubmed:abstractText
Time-lapse microscopy of human lung cancer (H460) cells showed that the endogenous cannabinoid anandamide (AEA), the phyto-cannabinoid Delta-9-tetrahydrocannabinol (THC) and a synthetic cannabinoid HU 210 all caused morphological changes characteristic of apoptosis. Janus green assays of H460 cell viability showed that AEA and THC caused significant increases in OD 595 nm at lower concentrations (10-50 microM) and significant decreases at 100 microM, whilst HU 210 caused significant decreases at all concentrations. In rat heart mitochondria, all three ligands caused significant decreases in oxygen consumption and mitochondrial membrane potential. THC and HU 210 caused significant increases in mitochondrial hydrogen peroxide production, whereas AEA was without significant effect. All three ligands induced biphasic changes in either mitochondrial complex I activity and/or mitochondrial complex II-III activity. These data demonstrate that AEA, THC, and HU 210 are all able to cause changes in integrated mitochondrial function, directly, in the absence of cannabinoid receptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1090-2104
pubmed:author
pubmed:issnType
Electronic
pubmed:day
7
pubmed:volume
364
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
131-7
pubmed:meshHeading
pubmed-meshheading:17931597-Apoptosis, pubmed-meshheading:17931597-Arachidonic Acids, pubmed-meshheading:17931597-Cannabinoids, pubmed-meshheading:17931597-Carcinoma, Non-Small-Cell Lung, pubmed-meshheading:17931597-Cell Line, Tumor, pubmed-meshheading:17931597-Electron Transport Complex I, pubmed-meshheading:17931597-Electron Transport Complex II, pubmed-meshheading:17931597-Electron Transport Complex III, pubmed-meshheading:17931597-Humans, pubmed-meshheading:17931597-Hydrogen Peroxide, pubmed-meshheading:17931597-Lung Neoplasms, pubmed-meshheading:17931597-Membrane Potential, Mitochondrial, pubmed-meshheading:17931597-Mitochondria, pubmed-meshheading:17931597-Models, Biological, pubmed-meshheading:17931597-Oxygen Consumption, pubmed-meshheading:17931597-Polyunsaturated Alkamides, pubmed-meshheading:17931597-Receptors, Cannabinoid, pubmed-meshheading:17931597-Tetrahydrocannabinol
pubmed:year
2007
pubmed:articleTitle
Cannabinoid receptor agonists are mitochondrial inhibitors: a unified hypothesis of how cannabinoids modulate mitochondrial function and induce cell death.
pubmed:affiliation
School of Biomedical Sciences, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't