Green C J, Healing G, Simpkin S, Lunec J, Fuller B J
Comp Biochem Physiol B. 1986;85(1):113-7. doi: 10.1016/0305-0491(86)90230-0.
Rabbit kidneys were clamped and subjected to warm ischaemia for 60 or 120 min then reperfused with blood for 60 min or for 24 hr. Treated rabbits received desferrioxamine at 15 or 50 mg/kg i.v. 15 min before reperfusion. Their kidneys were then removed and assayed for phospholipid Schiff base fluorescence (ex. 360 nm, em. 435 nm), diene and triene conjugates by UV spectrophotometry (240 nm and 268 nm respectively), for superoxide dismutase and for reduced and oxidised glutathione to provide an index of glutathione redox activity. All indices of lipid peroxidation were significantly elevated in untreated rabbits and glutathione redox activity was reduced. Treatment with desferrioxamine however effectively prevented these deviations and in many cases maintained them at the levels in fresh rabbit kidneys. These data provide further evidence that lipid peroxidation occurring during the reperfusion period is superimposed on the damage set up during warm ischaemia and may be preventable by administration of suitable therapeutic agents.
将兔肾钳夹并进行60或120分钟的热缺血，然后再灌注血液60分钟或24小时。在再灌注前15分钟，给处理过的兔子静脉注射15或50毫克/千克的去铁胺。然后取出它们的肾脏，通过紫外分光光度法（分别为240纳米和268纳米）检测磷脂席夫碱荧光（激发波长360纳米，发射波长435纳米）、二烯和三烯共轭物，检测超氧化物歧化酶以及还原型和氧化型谷胱甘肽，以提供谷胱甘肽氧化还原活性指标。在未处理的兔子中，所有脂质过氧化指标均显著升高，谷胱甘肽氧化还原活性降低。然而，用去铁胺治疗有效地预防了这些偏差，并且在许多情况下将它们维持在新鲜兔肾的水平。这些数据进一步证明，再灌注期间发生的脂质过氧化叠加在热缺血期间造成的损伤之上，并且可以通过给予合适的治疗药物来预防。
