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Vaccenic acid ( t 11–18∶1) is converted to c 9, t 11‐CLA in MCF‐7 and SW480 cancer cells
Author(s) -
Miller Aine,
McGrath Emma,
Stanton Catherine,
Devery Rosaleen
Publication year - 2003
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/s11745-003-1107-8
Subject(s) - cell culture , apoptosis , viability assay , cell growth , incubation , arachidonic acid , clinical chemistry , biochemistry , microbiology and biotechnology , chemistry , biology , endocrinology , genetics , enzyme
The aims of this study were to determine whether vaccenic acid (VA; t 11–18∶1) is converted to c 9, t 11‐CLA in human mammary (MCF‐7) and colon (SW480) cancer cell lines and whether VA influences cell viability and other CLA‐bioresponsive markers. When cells were incubated in the presence of VA at concentrations of 5 to 20 μg/mL, both VA and c 9, t 11‐CLA increased in cellular lipids in a dose‐dependent manner. After 4 d of incubation of SW480 and MCF‐7 cells with VA (20 μg/mL), c 9, t 11‐CLA increased from undetectable levels to 8.57 and 12.14 g/100 g FAME in cellular lipids, respectively. VA supplementation for 4 d at 5, 10, and 15 μg/mL had no effect on cell growth, whereas 20 μg/mL significantly ( P <0.05) reduced cell growth in both cell lines. VA (20 μg/mL) treatment induced DNA fragmentation and significantly ( P <0.05) depeleted cytosolic GSH levels in the SW480 cell line after 4 d of incubation, suggesting that apoptosis was the mode of cell death induced by VA. Both VA and c 9, t 11‐CLA reduced ( P <0.05) total ras expression in SW480 cells. 14 C‐Arachidonic acid uptake into the MG fraction was significantly increased ( P <0.05) in both cell lines while uptake into the phospholipid fraction decreased in response to VA. VA treatment significantly ( P <0.05) increased 8‐epi‐prostaglandin F 2α in both cell lines. The data indicate that growth suppression and cellular responses of both cells lines are likely mediated by VA desaturation to c 9, t 11‐CLA via Δ 9 ‐desaturase.