Grune T, Siems W G, Schneider W
Clinic of Physiotherapy, Medical Faculty (Charité), Humboldt University, Berlin, Germany.
Free Radic Biol Med. 1993 Aug;15(2):125-32. doi: 10.1016/0891-5849(93)90051-u.
The accumulation of the aldehydic lipid peroxidation product 4-hydroxynonenal and thiobarbituric acid-reactive substances was demonstrated during anoxia/reoxygenation of isolated rat hepatocytes. 4-Hydroxynonenal was detected as dinitrophenylhydrazone derivative by means of an isocratic HPLC separation. The highest 4-hydroxynonenal level was found 15 min after the beginning of reoxygenation. The concentration of 4-hydroxynonenal was compared with the thiobarbituric acid-reactive substances formation, the glutathione status, and the cell viability. Addition of the xanthine oxidase inhibitor oxypurinol decreased the aldehyde formation during the reoxygenation phase. The same suppression of oxidative load by 20 microM oxypurinol (inhibition of xanthine oxidase) and by 1 mM oxypurinol (inhibition of xanthine oxidase plus radical scavenging) leads to two conclusions: First, the purine degradation is the primary radical source of postanoxic hepatocytes; second, the inhibition of radical generation by xanthine oxidase is the main component of cell protecting by oxypurinol. On the other hand, oxypurinol addition did not accelerate the adenosine 5'-triphosphate (ATP) restoration.
在离体大鼠肝细胞缺氧/复氧过程中，醛类脂质过氧化产物4-羟基壬烯醛和硫代巴比妥酸反应性物质出现了蓄积。通过等度高效液相色谱分离法，将4-羟基壬烯醛检测为二硝基苯腙衍生物。复氧开始15分钟后，4-羟基壬烯醛水平达到最高。将4-羟基壬烯醛的浓度与硫代巴比妥酸反应性物质的形成、谷胱甘肽状态以及细胞活力进行了比较。添加黄嘌呤氧化酶抑制剂氧嘌呤醇可降低复氧阶段醛类的形成。20微摩尔氧嘌呤醇（抑制黄嘌呤氧化酶）和1毫摩尔氧嘌呤醇（抑制黄嘌呤氧化酶加自由基清除）对氧化负荷的相同抑制作用得出两个结论：第一，嘌呤降解是缺氧后肝细胞自由基的主要来源；第二，黄嘌呤氧化酶对自由基生成的抑制是氧嘌呤醇细胞保护作用的主要成分。另一方面，添加氧嘌呤醇并未加速三磷酸腺苷（ATP）的恢复。
