Santanam N, Sanchez R, Hendler S, Parthasarathy S
Department of Gynecology and Obstetrics, Emory University School of Medicine, Atlanta, GA 30322, USA.
FEBS Lett. 1997 Sep 15;414(3):549-51. doi: 10.1016/s0014-5793(97)01067-3.
Oxidation of low density lipoprotein (LDL) by cigarette smoke has been considered a potential mechanism by which smoking may promote atherosclerosis. We report in this study that cigarette smoke extract (CSE) inhibited copper-induced oxidation of LDL suggesting the presence of antioxidants in CSE. It is currently believed that peroxidases may oxidize LDL in vivo and during such oxidations antioxidants become pro-oxidants. Accordingly, when LDL was oxidized by peroxidase in the presence of CSE there was an increase in the oxidation of LDL. This is the first study suggesting that smoking may promote atherosclerosis by enhancing peroxidase-catalyzed lipid peroxidation.
香烟烟雾对低密度脂蛋白（LDL）的氧化作用被认为是吸烟促进动脉粥样硬化的一种潜在机制。我们在本研究中报告，香烟烟雾提取物（CSE）抑制了铜诱导的LDL氧化，这表明CSE中存在抗氧化剂。目前认为，过氧化物酶可能在体内氧化LDL，并且在这种氧化过程中抗氧化剂会变成促氧化剂。因此，当在CSE存在的情况下LDL被过氧化物酶氧化时，LDL的氧化增加。这是第一项表明吸烟可能通过增强过氧化物酶催化的脂质过氧化作用促进动脉粥样硬化的研究。
