Burke Anne, Fitzgerald Garret A
Gastrointestinal Division and the Center for Experimental Therapeutics, Hospital of the University of Pennsylvania, Philadelphia, PA 19104-6084, USA.
Prog Cardiovasc Dis. 2003 Jul-Aug;46(1):79-90. doi: 10.1016/s0033-0620(03)00076-8.
The relative importance of mechanisms relevant to smoking-induced vascular injury is poorly understood. Cigarette smoke is a source of free radicals but also results in cellular activation and consequent generation of free radicals in vivo. Here we consider several approaches to estimating the consequences of free radical generation in vivo, using measurements of modified lipids, proteins, and DNA. Smoking appears to result in elevation of several biomarkers of oxidant stress, some in a dose-related fashion. There is also some evidence that disordered endothelial function in smokers may be partly attributable to oxidant stress. Other effects of smoking on hemostatic activation, sympathoadrenal function, and lipoprotein structure and function may also be modulated by smoking-induced oxidant stress. The emergence and application of rational quantitatively reliable indexes of oxidant stress in vivo is likely to elucidate the relative contribution of oxidant stress to smoking-induced vascular injury.
与吸烟诱导的血管损伤相关机制的相对重要性目前仍知之甚少。香烟烟雾是自由基的一个来源，但同时也会导致细胞活化，进而在体内产生自由基。在此，我们通过测量修饰的脂质、蛋白质和DNA，探讨了几种评估体内自由基生成后果的方法。吸烟似乎会导致多种氧化应激生物标志物升高，其中一些呈现剂量相关模式。也有证据表明，吸烟者内皮功能紊乱可能部分归因于氧化应激。吸烟对止血激活、交感肾上腺功能以及脂蛋白结构和功能的其他影响，也可能受到吸烟诱导的氧化应激调节。体内合理且定量可靠的氧化应激指标的出现和应用，可能会阐明氧化应激在吸烟诱导的血管损伤中的相对作用。
