The effects of dietary conjugated linoleic acid (CLA) on fatty acid composition, lipid oxidation, and pork quality were investigated. Pigs (n = 20) were fed a diet containing 0, 1, 2.5, or 5% CLA for 4 wk and slaughtered at 105 kg. The longissimus thoracis et lumborum muscle was collected at 24 h postmortem. Pork loin chops (3 cm thick) were packaged aerobically and stored at 4 degrees C for 7 d. Samples were analyzed for ultimate pH, intramuscular fat content, fatty acid composition, thiobarbituric acid-reactive substances, color (L*, a*, b*), and water-holding capacity. Dietary CLA reduced the concentration of linoleic acid and increased CLA concentration in intramuscular fat of pork loin (P < 0.05). The concentration of CLA in muscle was increased with dietary CLA level and did not change during storage. Thiobarbituric acid-reactive substance value of control was higher than that of the CLA-fed groups (P < 0.05). Intramuscular fat content was increased by dietary CLA, and less purge loss was observed with samples from CLA-fed pigs (P < 0.05). Dietary CLA improved the color stability of pork loin during cold storage. After 7 d, lightness (L*) and yellowness (b*) of the 5% CLA-fed group were significantly lower than those of control (P < 0.05). The results indicated that the water-holding capacity of pork loin was increased with increased intramuscular fat content apparently caused by dietary CLA. Also, the data indicated that color stability of pork was improved with inhibition of lipid oxidation and changing of fatty acid composition by dietary CLA.
A commercially available mixture of conjugated linoleic acid (CLA) isomers decreases colon cancer cell growth. We compared the individual potencies of the two main isomers in this mixture [cis-9,trans-11 (c9t11) and trans-10,cis-12 (t10c12)] and assessed whether decreased cell growth is related to changes in secretion of insulin-like growth factor II (IGF-II) and/or IGF-binding proteins (IGFBPs), which regulate Caco-2 cell proliferation. Cells were incubated in serum-free medium with different concentrations of the individual CLA isomers. t10c12 CLA dose dependently decreased viable cell number (55 +/- 3% reduction 96 h after adding 5 microM t10c12 CLA). t10c12 CLA induced apoptosis and decreased DNA synthesis, whereas c9t11 CLA had no effect. Immunoblot analysis of 24-h serum-free conditioned medium using a monoclonal anti-IGF-II antibody revealed that Caco-2 cells secreted both a mature 7,500 molecular weight (M(r)) IGF-II and higher M(r) forms of IGF-II. The levels of the higher M(r) and the mature form of IGF-II were decreased 50 +/- 3% and 22 +/- 2%, respectively, by 5 microM t10c12 CLA. c9t11 CLA had no effect. Ligand blot analysis of conditioned medium using 125I-labeled IGF-II revealed that t10c12 CLA slightly decreased IGFBP-2 production; c9t11 CLA had no effect. Exogenous IGF-II reversed t10c12 CLA-induced growth inhibition and apoptosis. These results indicate that CLA-inhibited Caco-2 cell growth is caused by t10c12 CLA and may be mediated by decreasing IGF-II secretion in Caco-2 cells.
The growth inhibitory effect of a mixture of trans, trans conjugated linoleic acid isomers (t, t CLA) was investigated in a human breast cancer cell line, MCF-7, with references to c9, t11 CLA, t10, c12 CLA, and linoleic acid. The t, t CLA treatment effectively induced a cytotoxic effect in a time-dependent (0-6 days) and concentration-dependent (0-40 microM) manner, as compared to the reference and control treatments. The apoptotic parameters were measured on cells treated with 40 microM t, t CLA for 4 days. The occurrence of the characteristic morphological changes and DNA fragmentation confirmed apoptosis. The t, t CLA treatment led to an increase in the level of p53 tumor suppressor protein and Bax protein, but suppressed the expression of Bcl-2 protein. In addition, cytochrome c was released from the mitochondria into the cytosol, and the activation of caspase-3 led to the cleavage of poly(ADP-ribose) polymerase (PARP). Moreover, the composition of the linoleic and arachidonic acids was decreased in cellular membranes. These findings suggest that incorporation of t, t CLA in the membrane induces a mitochondria-mediated apoptosis that can enhance the antiproliferative effect of t, t CLA in MCF-7 cells.
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