Tan S, Gelman S, Wheat J K, Parks D A
Department of Pediatrics, University of Alabama at Birmingham 35233, USA.
South Med J. 1995 Apr;88(4):479-82. doi: 10.1097/00007611-199504000-00021.
Reactive oxygen species (ROS) generated from xanthine oxidase (XO) play an important role in ischemia-induced injury. We hypothesize that XO and xanthine dehydrogenase (XDH) are released into the circulation with ischemia reperfusion to the human liver and intestine. Blood was drawn from a patient, before and at intervals after an aortic cross-clamp procedure. Plasma was incubated in the presence of xanthine, with NAD+ (for XD +XO) and without NAD+ (for XO). The amount of urate formed was quantified using a high-performance liquid chromatograph (HPLC). The calculated XDH+XO and XO activity increased from 1.88 and 1.66 microU/mg protein, respectively, before the cross clamp to 3.77 and 3.11 microU/mg, respectively, 7 minutes after reperfusion to the superior mesenteric, celiac, and right renal artery beds. The release of a significant biological source of ROS may explain the damage to lung or heart observed after ischemia to the human liver and intestine.
由黄嘌呤氧化酶（XO）产生的活性氧（ROS）在缺血性损伤中起重要作用。我们推测，在人肝脏和肠道缺血再灌注时，XO和黄嘌呤脱氢酶（XDH）会释放到循环系统中。在主动脉交叉钳夹手术前及术后每隔一段时间从一名患者身上采血。血浆在黄嘌呤存在的情况下，分别添加NAD +（用于检测XD + XO）和不添加NAD +（用于检测XO）进行孵育。使用高效液相色谱仪（HPLC）对生成的尿酸量进行定量。计算得出，在肠系膜上动脉、腹腔动脉和右肾动脉床再灌注7分钟后，XDH + XO和XO活性分别从交叉钳夹前的1.88和1.66微单位/毫克蛋白增加到3.77和3.11微单位/毫克。ROS的一个重要生物来源的释放可能解释了人肝脏和肠道缺血后观察到的肺或心脏损伤。
