Roldán E J, Pinus C R, Turrens J F, Boveris A
Department of Biological Chemistry, Faculty of Pharmacy and Biochemistry, University of Buenos Aires, Argentina.
Gut. 1989 Feb;30(2):184-7. doi: 10.1136/gut.30.2.184.
Low level chemiluminescence of exposed rat intestine was measured during occlusive ischaemia and reperfusion. Spontaneous emission of in vivo rat intestine (10 +/- 1 cps/cm2) decreased almost to zero in animals subjected to ischaemia and when the period of ischaemia lasted only two minutes, chemiluminescence increased beyond control levels (39%, three minutes after reperfusion) at intestine deligation. This overshoot did not occur when rats were pretreated with allopurinol (40 + 100 mg/kg bw). The ratio of xanthine dehydrogenase to xanthine oxidase activities was 3.46 in preischaemic intestine samples. The same ratio was changed to 0.35 in samples subjected to two minutes of ischaemia. As chemiluminescence appears to reflect the steady state level of singlet oxygen, which in turn derives from the steady state level of peroxy radicals, these results agree with the view that oxygen radicals derived from the xanthine oxidase reaction are involved in the cellular damage produced after ischaemia and reoxygenation in the intestine.
在大鼠肠管闭塞性缺血和再灌注过程中，测定了暴露的大鼠肠管的低水平化学发光。在遭受缺血的动物中，体内大鼠肠管的自发发射（10±1 cps/cm²）几乎降至零，并且当缺血持续仅两分钟时，在肠管结扎处，化学发光在再灌注三分钟后增加至超过对照水平（39%）。当用别嘌呤醇（40 + 100 mg/kg体重）预处理大鼠时，这种过冲现象并未发生。在缺血前的肠管样本中，黄嘌呤脱氢酶与黄嘌呤氧化酶活性的比率为3.46。在经历两分钟缺血的样本中，相同的比率变为0.35。由于化学发光似乎反映了单线态氧的稳态水平，而单线态氧又源自过氧自由基的稳态水平，这些结果与以下观点一致，即源自黄嘌呤氧化酶反应的氧自由基参与了肠管缺血和再氧合后产生的细胞损伤。
