Carcinogenesis Advance Access published online on February 12, 2004
Carcinogenesis, doi:10.1093/carcin/bgh109
© 2004 by Oxford University Press
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MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION
1 Food & Biodynamic Chemistry Lab., Graduate School of Life Science and Agriculture, Tohoku University, Sendai, 981-8555, Japan
* Corresponding author. E-mail: miyazawa{at}biochem.tohoku.ac.jp.
Received 11 November 2003
; revised 26 January 2004
; accepted 3 February 2004
We have previously shown that conjugated linolenic acids (CLnA) prepared by alkaline isomerization have a stronger antitumor effect than conjugated linoleic acids (CLA). In this study, we compared the suppressive effect on tumor growth of
eleostearic acid, conjugated linoleic acid, tung oil, conjugated fatty acid, lipid peroxidation
Tumor growth suppression by
-eleostearic acid, a linolenic acid isomer with a conjugated triene system, via lipid peroxidation
-eleostearic acid (
-ESA, 9Z11E13E-18:3) with those of the CLA isomers 9Z11E-CLA and 10E12Z-CLA, using nude mice into which DLD-1 human colon cancer cells were transplanted. The results showed that
-ESA, which is a conjugated linolenic acid that can be prepared from natural sources in bulk, had a stronger antitumor effect than CLA. DNA fragmentation was enhanced and lipid peroxidation was increased in tumor tissues of the
-ESA-fed mice, which suggested that
-ESA induced apoptosis via lipid peroxidation. Furthermore, treatment of DLD-1 cells with
-ESA, 9Z11E-CLA and 10E12Z-CLA confirmed that
-ESA had a stronger antitumor effect than CLA in cultured cell lines. The induction of apoptosis by
-ESA was consistent with enhanced DNA fragmentation, increased caspase activity and increased expression of caspase mRNA following
-ESA treatment. Addition of
-tocopherol, an antioxidant, suppressed oxidative stress and apoptosis, suggesting that these effects were associated with lipid peroxidation.![]()
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