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黄嘌呤氧化酶在心肌缺血期间会造成损伤吗?

Does xanthine oxidase cause damage during myocardial ischemia?

作者信息

De Jong J W, van der Meer P, Huizer T, Serruys P W, Bos E, Roelandt J R

机构信息

Department of Cardiology, Erasmus University Rotterdam, The Netherlands.

出版信息

Bratisl Lek Listy. 1991 Jan;92(1):41-7.

PMID:2021865
Abstract

Xanthine oxidase is the pathological form of xanthine oxidoreductase, which generates free oxygen radicals, when it converts (hypo)xanthine to urate. We studied 1. developmental changes in rat heart, 2. urate production in catheterized patients, and 3. species differences of cardiac xanthine oxidase. First, we measured the activity of the enzyme at various ages. In rat-heart homogenate, xanthine oxidoreductase increased from 0.5 mU/g (newborn) to 25 mU/g (15 weeks, P less than 0.001). In the second part of the study, we demonstrated that patients undergoing coronary angioplasty showed some cardiac urate production. In the last part of our investigations we showed that in explanted human hearts perfused with hypoxanthine, the enzymatic activity was low, contrasting findings in some other species. The apparent xanthine oxidoreductase activity (mU/g) was: 33 (mouse), 28 (rat), 14 (guinea pig), 0.59 (rabbit), less than 0.1 (pig), 0.31 (man) and 3.7 (cow). We conclude that in several species, cardiac damage due to xanthine oxidase cannot be excluded; however in man it is unlikely to occur.

摘要

黄嘌呤氧化酶是黄嘌呤氧化还原酶的病理形式,当它将(次)黄嘌呤转化为尿酸盐时会产生游离氧自由基。我们研究了:1. 大鼠心脏的发育变化;2. 导管插入术患者的尿酸盐生成;3. 心脏黄嘌呤氧化酶的物种差异。首先,我们测量了不同年龄时该酶的活性。在大鼠心脏匀浆中,黄嘌呤氧化还原酶的活性从0.5 mU/g(新生大鼠)增加到25 mU/g(15周龄,P<0.001)。在研究的第二部分,我们证明接受冠状动脉血管成形术的患者会产生一些心脏尿酸盐。在我们研究的最后一部分,我们发现用次黄嘌呤灌注的离体人心脏中酶活性较低,这与其他一些物种的研究结果形成对比。黄嘌呤氧化还原酶的表观活性(mU/g)分别为:33(小鼠)、28(大鼠)、14(豚鼠)、0.59(兔)、<0.1(猪)、0.31(人)和3.7(牛)。我们得出结论,在几个物种中,不能排除黄嘌呤氧化酶导致心脏损伤的可能性;然而在人类中不太可能发生。

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