van de Poll Marcel C G, Dejong Cornelis H C, Fischer Marc A J G, Bast Aalt, Koek Ger H
Department of Surgery, University Hospital Maastricht & Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, 6200 AZ Maastricht, The Netherlands.
Clin Sci (Lond). 2008 Apr;114(8):553-60. doi: 10.1042/CS20070317.
Oxidative stress mediates cell injury during ischaemia/reperfusion. On the other hand, experimental findings suggest that ROS (reactive oxygen species) induce processes leading to ischaemic preconditioning. The extent and source of oxidative stress and its effect on antioxidant status in the human liver during intermittent ischaemia and reperfusion remains ill-defined. Therefore the aim of the present study was to investigate the occurrence of oxidative stress in humans undergoing liver resection. Liver biopsies, and arterial and hepatic venous blood samples were taken from ten patients undergoing hepatectomy with an intermittent Pringle manoeuvre. Plasma MDA (malondialdehyde) and hepatic GSSG levels were measured as markers of oxidative stress and plasma uric acid as a marker of xanthine oxidase activity. In addition, changes in hepatosplanchnic consumption of plasma antioxidants and hepatic levels of carotenoids and glutathione (GSH) were measured. After ischaemia, hepatosplanchnic release of MDA and increased hepatic GSSG levels were found. This was accompanied by the release of uric acid, reflecting xanthine oxidase activity. During reperfusion, ongoing oxidative stress was observed by further increases in hepatic GSSG content and hepatosplanchnic MDA release. Uric acid release was minimal during reperfusion. A gradual decrease in plasma antioxidant capacity and net hepatosplanchnic antioxidant uptake was observed upon prolonged cumulative ischaemia. Oxidative stress occurs during hepatic ischaemia in man mainly due to xanthine oxidase activity. Interestingly, the gradual decline in plasma antioxidant capacity and net hepatosplanchnic antioxidant uptake during prolonged cumulative ischaemia, preserved both hydrophilic and lipophilic hepatic antioxidant levels. Decreasing plasma levels and net hepatosplanchnic uptake of plasma antioxidants may warrant antioxidant supplementation, although it should be clarified to what extent limitation of oxidative stress compromises ROS-dependent pathways of ischaemic preconditioning.
氧化应激介导缺血/再灌注期间的细胞损伤。另一方面,实验结果表明活性氧(ROS)可诱导导致缺血预处理的过程。间歇性缺血和再灌注期间人体肝脏氧化应激的程度、来源及其对抗氧化状态的影响仍不明确。因此,本研究的目的是调查接受肝切除术患者体内氧化应激的发生情况。对10例行肝切除术并采用间歇性Pringle手法的患者进行肝活检,并采集动脉血和肝静脉血样本。测定血浆丙二醛(MDA)和肝脏谷胱甘肽二硫化物(GSSG)水平作为氧化应激标志物,测定血浆尿酸作为黄嘌呤氧化酶活性标志物。此外,还测定了肝内脏器对血浆抗氧化剂的消耗变化以及肝脏类胡萝卜素和谷胱甘肽(GSH)水平。缺血后,发现肝内脏器释放MDA且肝脏GSSG水平升高。这伴随着尿酸的释放,反映了黄嘌呤氧化酶的活性。再灌注期间,通过肝脏GSSG含量进一步升高和肝内脏器MDA释放增加观察到持续的氧化应激。再灌注期间尿酸释放极少。长时间累积缺血后,观察到血浆抗氧化能力和肝内脏器净抗氧化剂摄取逐渐下降。人体肝脏缺血期间发生氧化应激主要是由于黄嘌呤氧化酶的活性。有趣的是,长时间累积缺血期间血浆抗氧化能力和肝内脏器净抗氧化剂摄取的逐渐下降,使亲水性和脂溶性肝脏抗氧化剂水平均得以保留。血浆抗氧化剂水平降低和肝内脏器对血浆抗氧化剂的净摄取量减少可能需要补充抗氧化剂,尽管应明确氧化应激的限制在多大程度上会损害缺血预处理的ROS依赖性途径。