Southard J H, Marsh D C, McAnulty J F, Belzer F O
Surgery. 1987 May;101(5):566-70.
It has been suggested that the generation of oxygen-derived free radicals during the reperfusion of injured tissue causes organ dysfunction. The mechanism apparently involves the xanthine oxidase (XOD) enzyme system, which becomes activated during reperfusion and generates oxygen-derived free radicals faster than their dismutation by naturally occurring superoxide dismutase (SOD). In this study, we measured the XOD and SOD activities of liver and kidney tissue in species used for organ preservation studies (rats, dogs, and human beings). We also measured the effect that up to 5 days of hypothermic preservation has on the activity of SOD and XOD in canine kidneys and expressed activities as the ratio of SOD to XOD; large ratios suggest lower susceptibility to oxygen-derived free radical damage. The SOD:XOD ratios for rat tissue were consistently lower (kidney = 2.7 X 10(4), liver = 8.9 X 10(3)) than for canine tissue (kidney = 7.0 X 10(5), liver = 4.1 X 10(4)) and human tissue (kidney = 1.1 X 10(6), liver = 6.4 X 10(5)). Canine kidneys perfused for 3 days showed no change in SOD:XOD ratio. After 5 days of perfusion, the SOD:XOD ratio decreased by 50% but was still quite large (5 X 10(5]. This high SOD:XOD ratio in canine and human tissues suggests that they may be less sensitive to oxygen-derived free radical damage than rat tissues.
有人提出，受损组织再灌注过程中氧衍生自由基的产生会导致器官功能障碍。其机制显然涉及黄嘌呤氧化酶（XOD）酶系统，该系统在再灌注过程中被激活，产生氧衍生自由基的速度比天然存在的超氧化物歧化酶（SOD）使其歧化的速度更快。在本研究中，我们测量了用于器官保存研究的物种（大鼠、狗和人类）肝脏和肾脏组织的XOD和SOD活性。我们还测量了长达5天的低温保存对犬肾中SOD和XOD活性的影响，并将活性表示为SOD与XOD的比值；比值大表明对氧衍生自由基损伤的敏感性较低。大鼠组织的SOD:XOD比值始终低于犬组织（肾脏=7.0×10⁵，肝脏=4.1×10⁴）和人类组织（肾脏=1.1×10⁶，肝脏=6.4×10⁵）（肾脏=2.7×10⁴，肝脏=8.9×10³）。灌注3天的犬肾SOD:XOD比值无变化。灌注5天后，SOD:XOD比值下降了50%，但仍然相当大（5×10⁵）。犬和人类组织中这种高SOD:XOD比值表明，它们可能比大鼠组织对氧衍生自由基损伤更不敏感。
