Incorporation and effect of arachidonic acid on the growth of the human K562 cell line

Lipoxygenase inhibitors reduce the growth of K562 cells (chronic myelogenous human leukaemia blasts) suggesting a role for endogenous lipoxygenase products of arachidonic acid (AA) in their proliferation. The objectives of this work are to investigate the incorporation of AA into K562 cells and to a...

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Bibliographic Details
Published in:Cancer letters 1999-05, Vol.139 (1), p.75-78
Main Authors: Denizot, Y., Dulery, C., Desplat, V., Praloran, V.
Format: Article
Language:English
Subjects:
Acylation
Arachidonic acid
Arachidonic Acid - pharmacology
Biological and medical sciences
Carcinogenesis, carcinogens and anticarcinogens
Cell Division - drug effects
Cell Membrane - drug effects
Cell proliferation
Chemical agents
Chromatography
Deoxyribonucleic acid
DNA
Experiments
Fatty acids
Humans
Iodine
K562 Cells
Lecithin
Leukemia
Leukotriene B4
Lipoxygenase
Lipoxygenase - metabolism
Lipoxygenase - pharmacology
Lipoxygenase metabolites
Medical sciences
Metabolites
Phosphatidylcholine
Phosphatidylethanolamine
Phospholipase A2
Phospholipids
Proliferation
Solvents
Thymidine
Time Factors
Triglycerides
Tumors
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Summary:Lipoxygenase inhibitors reduce the growth of K562 cells (chronic myelogenous human leukaemia blasts) suggesting a role for endogenous lipoxygenase products of arachidonic acid (AA) in their proliferation. The objectives of this work are to investigate the incorporation of AA into K562 cells and to assess the effects of the exogenous addition of AA and lipoxygenase products on their growth. The mechanism of acylation of [3H]-AA indicates that K562 cells incorporate AA into their membrane phospholipids and triglycerides. PLA2-treatment and base hydrolysis experiments confirm that [3H]-AA is incorporated unmodified into K562 phospholipids and is linked by an ester bond. Prelabelling-chase experiments indicate a transfer of labelled AA from phosphatidylcholine to phosphatidylethanolamine. The addition of AA and lipoxygenase products of AA (leukotriene B4 and C4, lipoxin B4, 12-hydroxyeicosatetraenoic acid (12-HETE) and 15-HETE) has no effect on K562 cell proliferation assessed by [3H]thymidine incorporation into DNA. In conclusion, while K562 cells readily incorporate AA into their membrane phospholipids and triglycerides, AA and lipoxygenase products are not important modulators of their proliferation.
ISSN:0304-3835
1872-7980
DOI:10.1016/S0304-3835(99)00006-3