Alleviation of the cytotoxic activity induced by trans10, cis12-conjugated linoleic acid in rat hepatoma dRLh-84 cells by oleic or palmitoleic acid

Yamasaki, Masao; Chujo, Hitomi; Nou, Shinsuke; Tachibana, Hirofumi; Yamada, Koji

doi:10.1016/s0304-3835(03)00215-5

Cited by 17 publications

(10 citation statements)

References 20 publications

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“…However, recent in vitro studies [13,18,19] showed that t10,c12-CLA is somewhat more efficacious than c9,t11-CLA for many parameters, suggesting the possibility that lower doses of t10,c12-CLA can be utilized in vivo, with good efficacy and low toxicity. The results in Fig.…”

Section: Discussionmentioning

confidence: 99%

Potent inhibitory effect of trans9, trans11 isomer of conjugated linoleic acid on the growth of human colon cancer cells

Beppu

Hosokawa

Tanaka

et al. 2006

The Journal of Nutritional Biochemistry

122

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This study compared the growth inhibitory effects of pure conjugated linoleic acid (CLA) isomers (cis(c)9,c11-CLA, c9,trans(t)11-CLA, t9,t11-CLA, and t10,c12-CLA) on human colon cancer cell lines (Caco-2, HT-29, and DLD-1). When Caco-2 cells were incubated up to 72 h with 200 M each isomer even in the presence of 10% fetal bovine serum (FBS), cell proliferation was inhibited by all CLA isomers in a time dependent manner. The strongest inhibitory effect was shown by t9,t11-CLA, followed by t10,c12-CLA, c9,c11-CLA, and c9,t11-CLA, respectively. The strongest effect of t9,t11-CLA was also observed in other colon cancer cell lines (HT-29 and DLD-1). The order of the inhibitory effect of CLA isomer was confirmed in the presence of 1% FBS. CLA isomers supplemented in the culture medium were readily incorporated into the cellular lipids of Caco-2 and changed their fatty acid composition. The CLA contents in cellular lipids were 26.2+2.7% for t9,t11-CLA, 35.9+0.3% for c9,t11-CLA, and 46.3+0.8% for t10,c12-CLA, respectively. DNA fragmentation was clearly recognized in Caco-2 cells treated with t9,t11-CLA. This apoptotic effect of t9,t11-CLA was dose-and time-dependent. DNA fragmentation was also induced by 9c,11t-CLA and t10,c12-CLA. However, fragmentation levels with both isomers were much lower than that with t9,t11-CLA.t9t11-CLA treatment of Caco-2 cells decreased Bcl-2 levels in association with apoptosis, whereas Bax levels remained unchanged. These results suggest that decreased expression of Bcl-2 by t9t11-CLA might increase the sensitivity of cells to lipid peroxidation and to programmed cell death, apoptosis. AbstractThis study compared the growth inhibitory effects of pure conjugated linoleic acid (CLA) isomers (cis(c)9,c11-CLA, c9,trans(t)11-CLA, t9,t11-CLA, and t10,c12-CLA) on human colon cancer cell lines (Caco-2, HT-29, and DLD-1). When Caco-2 cells were incubated up to 72 h with 200 µM each isomer even in the presence of 10% fetal bovine serum (FBS), cell proliferation was inhibited by all CLA isomers in a time dependent manner. The strongest inhibitory effect was shown by t9,t11-CLA, followed by t10,c12-CLA, c9,c11-CLA, and c9,t11-CLA, respectively. The strongest effect of t9,t11-CLA was also observed in other colon cancer cell lines (HT-29 and DLD-1). The order of the inhibitory effect of CLA isomer was confirmed in the presence of 1% FBS. * Manuscript 2CLA isomers supplemented in the culture medium were readily incorporated into the cellular lipids of Caco-2 and changed their fatty acid composition. The CLA contents in cellular lipids were 26.2+2.7% for t9,t11-CLA, 35.9+0.3% for c9,t11-CLA, and 46.3+0.8% for t10,c12-CLA, respectively. DNA fragmentation was clearly recognized in Caco-2 cells treated with t9,t11-CLA. This apoptotic effect of t9,t11-CLA was doseand time-dependent. DNA fragmentation was also induced by 9c,11t-CLA and t10,c12-CLA. However, fragmentation levels with both isomers were much lower than that with t9,t11-CLA. t9t11-CLA treatment of Caco-2 cells decreased Bcl-2 levels in...

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Section: Discussionmentioning

confidence: 99%

Potent inhibitory effect of trans9, trans11 isomer of conjugated linoleic acid on the growth of human colon cancer cells

Beppu

Hosokawa

Tanaka

et al. 2006

The Journal of Nutritional Biochemistry

122

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“…These studies suggested that t10, c12-conjugated linoleic acid could act as a highly effective antiliver cancer component. On the other hand, previous studies indicated that the apoptotic cell death induced by t10, c12-conjugated linoleic acid was modulated by other fatty acids (Igarashi and Miyazawa 2001;Yamasaki et al 2003). Here, we examined the effects of inhibitors of MAPKs and PI3K/Akt pathways on the effect of oleic acid because these signaling pathways are involved in cell survival, proliferation, and apoptotic cell death events.…”

Section: Introductionmentioning

confidence: 96%

“…Reduction of these fatty acids was recognized in various cell types, and this phenomenon has been explained by inhibition of stearoyl-CoA desaturase (Choi et al 2000;Park et al 2000). Supplementation of oleic acid or palmitoleic acid with t10, c12-conjugated linoleic acid completely abrogated the cytotoxicity of t10, c12-conjugated linoleic acid (Yamasaki et al 2003). Therefore, cytotoxicity of t10, c12-conjugated linoleic acid may be explained by the depletion of intracellular oleic acid and palmitoleic acid.…”

Section: Introductionmentioning

confidence: 99%

Oleic acid prevents apoptotic cell death induced by trans10, cis12 isomer of conjugated linoleic acid via p38 MAP kinase dependent pathway

Yamasaki

Tachibana

Yamada

et al. 2008

In Vitro Cell.Dev.Biol.-Animal

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Our previous study indicated that oleic acid prevented apoptotic cell death induced by trans10, cis12 (t10, c12)-conjugated linoleic acid in rat hepatoma dRLh-84 cells. The intracellular mechanism of action oleic acid is still unknown. Here, we showed that p38 mitogen-activated protein kinase (MAPK) inhibition using its specific inhibitor SB203580 cancelled the ameliorative effect of oleic acid on the cytotoxicity of t10, c12-conjugated linoleic acid. In addition, SubG1 cell population analysis showed that p38 MAPK played an essential role in the prevention of apoptotic cell death by oleic acid. In fact, p38 phosphorylation level was upregulated in cells treated with oleic acid irrespective of t10, c12-conjugated linoleic acid stimulation. Interestingly, t10, c12-conjugated linoleic acid increased intracellular triglyceride accumulation. However, oleic acid completely inhibited this effect. These observations indicated the involvement of blockade of a p38 MAPK pathway in the ameliorative effect of oleic acid on apoptosis induced by t10, c12-conjugated linoleic acid.

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“…A recent study revealed that JA has the most potent cytotoxic effects on human colon cancer cells 9 . On the other hand, other fatty acids such as linoleic acid LA , oleic acid, and palmitoleic acid, interfere with the cytotoxic effects of CLA on cancer cells 10,11 . This interaction is at least partially illustrated by the inhibitory effect of CLA on stearoyl-CoA desaturase SCD that mediates delta-9 desaturation of saturated fatty acids 11 .…”

Section: Introductionmentioning

confidence: 99%

Induction of Apoptotic Cell Death in HL-60 Cells by Jacaranda Seed Oil Derived Fatty Acids

et al. 2013

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Alleviation of the cytotoxic activity induced by trans10, cis12-conjugated linoleic acid in rat hepatoma dRLh-84 cells by oleic or palmitoleic acid

Cited by 17 publications

References 20 publications

Potent inhibitory effect of trans9, trans11 isomer of conjugated linoleic acid on the growth of human colon cancer cells

Potent inhibitory effect of trans9, trans11 isomer of conjugated linoleic acid on the growth of human colon cancer cells

Oleic acid prevents apoptotic cell death induced by trans10, cis12 isomer of conjugated linoleic acid via p38 MAP kinase dependent pathway

Induction of Apoptotic Cell Death in HL-60 Cells by Jacaranda Seed Oil Derived Fatty Acids

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