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Apoptosis
in human primary brain tumours: actions of arachidonic acid
Williams JR, Leaver HA, Ironside JW, Miller EP, Whittle IR, Gregor A
Department of Pharmacology, University of Edinburgh, UK
It has been postulated that loss of proliferative control in tumour cells is a
consequence of depletion of cellular arachidonic acid (AA) and that exogenous AA
and n-6 fatty acids may restore control of proliferation.
To test this hypothesis and to investigate the activity of AA, apoptosis in
human primary brain tumour cells was analysed using flow terminal
deoxynucleotide transferase uridine nick end-labelling (TUNEL).
The effect of exogenous AA (30 microM) was analysed in collagenase-dispersed
tissue from seven human primary brain tumours and in the normal brain tissue
surrounding one of the tumours.
Exogenous AA stimulated apoptosis in tumour tissue.
A rapid three-fold increase in endonuclease activity was detected in tumour
cells incubated with AA.
The increase in apoptosis was significantly greater than the contemporary (<
15%) increase in necrosis detected using propidium iodide permeability and was
greater than AA effects on normal brain tissue.
These results are consistent with activation of the pathways of apoptosis by AA.
PMID: 9610841 [PubMed - indexed for MEDLINE]
Source: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9610841&dopt=Abstract
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