Vaccenic acid (t11-18:1) is converted to c9,t11-CLA in MCF-7 and SW480 cancer cells.

The aims of this study were to determine whether vaccenic acid (VA; t11–18∶1) is converted to c9,t11-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 c9,t11-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), c9,t11-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 c9,t11-CLA reduced (P<0.05) total ras expression in SW480 cells. 14C-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 F2α in both cell lines. The data indicate that growth suppression and cellular responses of both cells lines are likely mediated by VA desaturation to c9,t11-CLA via Δ9-desaturase.