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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/17303


    Title: Trans Fatty Acids Enhanced beta-Amyloid Induced Oxidative Stress in Nerve Growth Factor Differentiated PC12 Cells
    Authors: Tsai, Shih-jei;Liu, Wen-hu;Yin, Mei-chin;殷梅津
    Contributors: 保健營養生技學系
    Keywords: Trans fatty acid;Amyloid;PC12 cells;Neurodegeneration;Mitochondrial dysfunction
    Date: 2012-01
    Issue Date: 2012-11-26 10:31:15 (UTC+8)
    Abstract: The effects of trans fatty acids, elaidic acid (trans-9, C18:1) and linoelaidic acid (trans-9, trans-12 C18:2), at 20 or 40 μM in nerve growth factor differentiated PC12 cells with or without beta-amyloid peptide (Aβ) were examined. Elaidic acid treatment alone did not affect cell viability and oxidative injury associated markers ( P > 0.05). However, co-treatments of elaidic acid and Aβ led to more reduction in mitochondrial membrane potential (MMP) and Na-K-ATPase activity, and more increase in DNA fragmentation and 8-hydroxydeoxyguanosine (8-OHdG) production than Aβ treatment alone ( P < 0.05). Linoelaidic acid alone exhibited apoptotic and oxidative effects in cells via decreasing MMP and Na-K-ATPase activity, increasing reactive oxygen species (ROS) level, lowering glutathione content and glutathione peroxidase (GPX) activity ( P < 0.05). The co-treatments of linoelaidic acid with Aβ further enhanced oxidative damage via enhancing the generation of ROS, nitrite oxide and 8-OHdG, elevating caspase-3, caspase-8 and nitric oxide synthase activities, as well as declining GPX, catalase and superoxide dismutase activities ( P < 0.05). These results suggested that the interaction of linoelaidic acid and Aβ promoted oxidative stress and impaired mitochondrial functions in neuronal cells.(trans-9, trans-12 C18:2), at 20 or 40 M in nerve growth factor differentiated PC12 cells
    with or without beta-amyloid peptide (A) were examined. Elaidic acid treatment alone
    did not affect cell viability and oxidative injury associated markers (P>0.05). However,
    co-treatments of elaidic acid and Aled to more reduction in mitochondrial membrane
    potential (MMP) and Na+
    -K
    +
    -ATPase activity, and more increase in DNA fragmentation
    and 8-hydroxydeoxyguanosine (8-OHdG) production than Atreatment alone (P<0.05).
    Linoelaidic acid alone exhibited apoptotic and oxidative effects in cells via decreasing
    MMP and Na+
    -K
    +
    -ATPase activity, increasing reactive oxygen species (ROS) level,
    lowering glutathione content and glutathione peroxidase (GPX) activity (P<0.05). The
    co-treatments of linoelaidic acid with A further enhanced oxidative damage via
    enhancing the generation of ROS, nitrite oxide and 8-OHdG, elevating caspase-3,
    caspase-8 and nitric oxide synthase activities, as well as declining GPX, catalase and
    superoxide dismutase activities (P<0.05). These results suggested that the interaction of
    linoelaidic acid and Apromoted oxidative stress and impaired mitochondrial functions in
    neuronal cells."
    Relation: NEUROCHEMICAL RESEARCH
    Appears in Collections:[食品營養與保健生技學系] 期刊論文

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