Kock R, Delvoux B, Sigmund M, Greiling H
Institute for Clinical Chemistry and Pathobiochemistry, Medical Faculty, University of Technology Aachen, Germany.
Eur J Clin Chem Clin Biochem. 1994 Nov;32(11):837-42. doi: 10.1515/cclm.1994.32.11.837.
The aim of this study was the elucidation of the role of the xanthine oxidoreductase in the purine metabolism in ischaemic diseases of man. The serum concentrations of hypoxanthine, xanthine, uric acid and allantoin were determined in peripheral blood samples from patients with angina pectoris, cerebral insult and myocardial infarction with thrombolytic therapy and were compared with the concentrations obtained for healthy males and females. No significant differences were observed for the serum hypoxanthine concentrations, xanthine concentrations, the sum (hypoxanthine+xanthine) and the ratio (xanthine/hypoxanthine) between the healthy males, healthy females, the patients suffering from angina pectoris and the patients suffering from cerebral insult. An increase of the serum xanthine concentration in patients with myocardial infarction indicates a significant metabolic involvement of xanthine oxidoreductase in this disease and therefore a possible role in the development of tissue damage in the postischaemic phase due to oxygen radicals generated by the oxidase activity of this enzyme. The serum concentrations of uric acid and allantoin showed no differences between any of the studied groups. Study of the non-enzymatic oxidation of uric acid to allantoin by oxygen radicals, a relevant radical-scavenging mechanism in other diseases, provided no indication of an increased concentration of oxygen radicals due to the xanthine oxidoreductase reaction or other radical-producing mechanisms.
本研究的目的是阐明黄嘌呤氧化还原酶在人类缺血性疾病嘌呤代谢中的作用。测定了接受溶栓治疗的心绞痛、脑损伤和心肌梗死患者外周血样本中次黄嘌呤、黄嘌呤、尿酸和尿囊素的血清浓度，并与健康男性和女性的浓度进行比较。在健康男性、健康女性、心绞痛患者和脑损伤患者之间，血清次黄嘌呤浓度、黄嘌呤浓度、总和（次黄嘌呤 + 黄嘌呤）以及比率（黄嘌呤/次黄嘌呤）均未观察到显著差异。心肌梗死患者血清黄嘌呤浓度的升高表明黄嘌呤氧化还原酶在该疾病中存在显著的代谢参与，因此可能在缺血后阶段由于该酶的氧化酶活性产生的氧自由基导致组织损伤的发展中发挥作用。尿酸和尿囊素的血清浓度在任何研究组之间均无差异。对尿酸通过氧自由基非酶氧化为尿囊素的研究（这是其他疾病中一种相关的自由基清除机制），未显示由于黄嘌呤氧化还原酶反应或其他自由基产生机制导致氧自由基浓度增加的迹象。
