Sermet A, Taşdemir N, Deniz B, Atmaca M
Department of Neurology, Faculty of Medicine, Dicle University, Diyarbakir, Turkey.
Cytobios. 2000;102(401):157-72.
Time-dependent changes in the activities of antioxidant enzymes and an oxidant enzyme, xanthine oxidase (XO), were detected in primary and peri-ischaemic brain regions during permanent occlusion of the middle cerebral artery (MCAO) in rats. There were no changes in superoxide dismutase (SOD) and catalase (CAT) activities after 3 h of MCAO, whereas antioxidant enzyme activities decreased significantly in ischaemic brain areas following 24 h of ischaemia. After 48 h, the enzyme activities returned to the baseline but then a further increase was observed in ischaemic brain areas by 72 h post-ischaemia. Normally, XO exists as a dehydrogenase (XD), but it is converted to XO which contributes to injury in some ischaemic tissues. The XO activity increased slightly at 3 h after ischaemia, but after 24 h of ischaemia it returned to the baseline and then remained relatively unchanged in ischaemic areas. Pretreatment with allopurinol before ischaemia prevented changes in SOD and CAT activities and attenuated brain oedema during 24 h of ischaemia. Neither XO nor XD activity changed in allopurinol-treated rats at the times of ischaemia. These results indicated that ischaemic brain tissue remained vulnerable to free radical damage for as long as 48 h after ischaemia, and XO was probably not an important source of free radicals in cerebral ischaemia.
在大鼠大脑中动脉永久性闭塞（MCAO）期间，检测了原发性和缺血周围脑区抗氧化酶和一种氧化酶——黄嘌呤氧化酶（XO）活性的时间依赖性变化。MCAO 3小时后，超氧化物歧化酶（SOD）和过氧化氢酶（CAT）活性无变化，而缺血24小时后，缺血脑区抗氧化酶活性显著降低。48小时后，酶活性恢复到基线水平，但在缺血后72小时，缺血脑区酶活性进一步升高。正常情况下，XO以脱氢酶（XD）形式存在，但它会转化为XO，在一些缺血组织中造成损伤。缺血3小时后XO活性略有增加，但缺血24小时后它恢复到基线水平，然后在缺血区域保持相对不变。缺血前用别嘌呤醇预处理可防止SOD和CAT活性变化，并减轻缺血24小时期间的脑水肿。在缺血时，别嘌呤醇处理的大鼠中XO和XD活性均未改变。这些结果表明，缺血脑组织在缺血后长达48小时内仍易受自由基损伤，并且XO可能不是脑缺血中自由基的重要来源。
