TY - JOUR
T1 - Tumor growth suppression by α-eleostearic acid, a linolenic acid isomer with a cunjugated triene system, via lipid peroxidation
AU - Tsuzuki, Tsuyoshi
AU - Tokuyama, Yoshiko
AU - Igarashi, Miki
AU - Miyazawa, Teruo
PY - 2004/8/1
Y1 - 2004/8/1
N2 - 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 have compared the suppressive effect on tumor growth of α-eleostearic acid (α-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 α-ESA, which is a CLnA 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 α-ESA-fed mice, which suggested that α-ESA induced apoptosis via lipid peroxidation. Furthermore, treatment of DLD-1 cells with α-ESA, 9Z11E-CLA and 10E12Z-CLA confirmed that α-ESA had a stronger antitumor effect than CLA in cultured cell lines. The induction of apoptosis by α-ESA was consistent with enhanced DNA fragmentation, increased caspase activity and increased expression of caspase mRNA following α-ESA treatment. Addition of α-tocopherol, an antioxidant, suppressed oxidative stress and apoptosis, suggesting that these effects were associated with lipid peroxidation.
AB - 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 have compared the suppressive effect on tumor growth of α-eleostearic acid (α-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 α-ESA, which is a CLnA 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 α-ESA-fed mice, which suggested that α-ESA induced apoptosis via lipid peroxidation. Furthermore, treatment of DLD-1 cells with α-ESA, 9Z11E-CLA and 10E12Z-CLA confirmed that α-ESA had a stronger antitumor effect than CLA in cultured cell lines. The induction of apoptosis by α-ESA was consistent with enhanced DNA fragmentation, increased caspase activity and increased expression of caspase mRNA following α-ESA treatment. Addition of α-tocopherol, an antioxidant, suppressed oxidative stress and apoptosis, suggesting that these effects were associated with lipid peroxidation.
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U2 - 10.1093/carcin/bgh109
DO - 10.1093/carcin/bgh109
M3 - Article
C2 - 14963014
AN - SCOPUS:4344715276
VL - 25
SP - 1417
EP - 1425
JO - Carcinogenesis
JF - Carcinogenesis
SN - 0143-3334
IS - 8
ER -