The inhibitory effect of conjugated dienoic derivatives (CLA) of linoleic acid on the growth of human tumor cell lines is in part due to increased lipid peroxidation.
We have examined the effects of linoleic acid, LA (18:2 n-6) and its naturally occurring conjugated derivatives (CLA) on the growth of three different lung adenocarcinoma cell lines (A-427, SK-LU-1, A549) and one human glioblastoma cell line (A-172). CLA exerted a dose dependent reduction in proliferation of the lung adenocarcinoma cell lines with A-427 being the most sensitive one, but had virtually no effect on A-172. In contrast, LA had no inhibitory effect on either cell line. A significant increase in lipid peroxidation (measured as formation of malondialdehyde, MDA) was observed after exposure of the lung adenocarcinoma cell lines to 40 microM CLA. This level was approximately 2-fold higher than after exposure to 40 microM LA. The formation of MDA was completely abolished by 30 microM vitamin E, but the growth rates were only partially restored, indicating that cytotoxic lipid peroxidation products are only in part responsible for the growth inhibitory effects of CLA.
Schønberg
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UNIGEN Center for Molecular Biology, University of Trondheim, Norway.
Krokan
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D000970:Antineoplastic Agents / Q000494:pharmacology*; D002455:Cell Division / Q000187:drug effects; D006801:Humans; D019787:Linoleic Acid; D008041:Linoleic Acids / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects*; D014407:Tumor Cells, Cultured; D014810:Vitamin E / Q000494:pharmacology
D000970:Antineoplastic Agents; D008041:Linoleic Acids; D014810:Vitamin E; D019787:Linoleic Acid