Hoerl Gerd, Ledinski Gerhard, Kager Gerd, Thalhammer Michael, Koestenberger Martin, Juergens Guenther, Gary Thomas, Cvirn Gerhard
Institute of Physiological Chemistry, Medical University of Graz, Harrachgasse 21/II, Graz A-8010, Austria.
Department of Surgery, Medical University of Graz, Graz, Austria.
Chem Phys Lipids. 2014 Dec;184:38-41. doi: 10.1016/j.chemphyslip.2014.09.004. Epub 2014 Sep 18.
Plaque formation is confined to the arterial trunk. We assumed that due to the higher aeration of arterial compared to venous blood, higher levels of the atherogenic agent oxidized LDL might be present in arteries, contributing to plaque formation. We aimed to compare (i) the basal oxidative status of LDL in arterial and venous blood and (ii) the susceptibility of arterial and venous LDL to oxidation. The basal oxidative status of LDL was determined by measuring lipid hydroperoxide (LPO) concentrations, plasma levels of auto-antibodies against oxidized LDL, and by measuring oxidation-specific epitopes on LDL particles. The oxidizability of arterial vs. venous LDL (catalyzed by copper) was estimated by monitoring the time-course of conjugated dienes formation. Interestingly, we found the same basal oxidative status of LDL in arterial and venous plasma. LPO concentrations and levels of auto-antibodies against oxidized LDL were similar in arterial and venous plasma and amounts of oxidation-specific epitopes were similar on the respective LDL particles. Moreover, we found similar susceptibilities of arterial and venous LDL to (copper-mediated) oxidation. Lag-times until the onset of conjugated diene formation were slightly shorter in arterial compared to venous LDL in the presence of 5 μM, but not in the presence of 1 μM CuCl2. Additionally, we found significantly higher levels of the atherogenic lipoprotein(a) in arterial plasma. We conclude that not higher oxidizability of arterial LDL but higher arterial lipoprotein(a) levels might help to explain why sclerosis is confined to the arterial trunk.
斑块形成局限于动脉主干。我们推测，由于动脉血比静脉血的含氧量更高，动脉中可能存在更高水平的致动脉粥样硬化因子氧化低密度脂蛋白（ox-LDL），这有助于斑块形成。我们旨在比较：（i）动脉血和静脉血中低密度脂蛋白（LDL）的基础氧化状态；（ii）动脉LDL和静脉LDL对氧化的敏感性。通过测量脂质过氧化氢（LPO）浓度、针对ox-LDL的自身抗体的血浆水平以及测量LDL颗粒上的氧化特异性表位来确定LDL的基础氧化状态。通过监测共轭二烯形成的时间进程来估计动脉LDL与静脉LDL（由铜催化）的氧化能力。有趣的是，我们发现动脉血浆和静脉血浆中LDL的基础氧化状态相同。动脉血浆和静脉血浆中LPO浓度以及针对ox-LDL的自身抗体水平相似，并且各自LDL颗粒上的氧化特异性表位数量也相似。此外，我们发现动脉LDL和静脉LDL对（铜介导的）氧化的敏感性相似。在存在5 μM铜离子的情况下，动脉LDL中直到共轭二烯形成开始的延迟时间比静脉LDL略短，但在存在1 μM CuCl2的情况下并非如此。此外，我们发现动脉血浆中致动脉粥样硬化的脂蛋白（a）水平显著更高。我们得出结论，并非动脉LDL的氧化能力更高，而是动脉中脂蛋白（a）水平更高，这可能有助于解释为什么硬化局限于动脉主干。
