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Antioxidative enzyme and glutathione S-transferase activities in diabetic rats exposed to long-term ASA treatment

机译：长期接受ASA治疗的糖尿病大鼠的抗氧化酶和谷胱甘肽S-转移酶活性

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Low-dose acetylsalicylic acid (ASA) treatment is a standard therapeutic approach in diabetes mellitus for prevention of long-term vascular complications. The aim of the present work was to investigate the effect of long-term ASA administration in experimental diabetes on activities of some liver enzymes: glutathione peroxidase (GSHPx), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione S-transferase (GST). Blood glucose, glycated hemoglobin, as well as plasma ALT and AST activities increased in rats with streptozotocin-induced experimental diabetes. The long-term hyperglycemia resulted in decreased activities of GSHPx (by 26%), catalase (by 34%), GST (by 38%) and G6PDH (by 27%) in diabetic animals. We did not observe increased accumulation of membrane lipid peroxidation products or altered levels of reduced glutathione in livers. The linear correlation between blood glucose and glycated hemoglobin in diabetic animals was distorted upon ASA treatment, which was likely due to a chemical competition between nonenzymatic protein glycosylation and protein acetylation. The long-term ASA administration partially reversed the decrease in GSHPx activity, but did not influence the activities of catalase and GST in diabetic rats. Otherwise, some decrease in these parameters was noted in ASA-treated nondiabetic animals. Increased ASA-induced G6PDH activity was recorded in both diabetic and nondiabetic rats. While both glycation due to diabetic hyperglycemia and ASA-mediated acetylation had very similar effects on the activities of all studied enzymes but G6PDH, we conclude that non-enzymatic modification by either glucose or ASA may be a common mechanism of the observed convergence. (c) 2006 Elsevier Inc. All rights reserved.
机译：低剂量乙酰水杨酸（ASA）治疗是糖尿病中预防长期血管并发症的标准治疗方法。本工作的目的是研究在实验性糖尿病中长期服用ASA对某些肝脏酶活性的影响：谷胱甘肽过氧化物酶（GSHPx），过氧化氢酶，葡萄糖6-磷酸脱氢酶（G6PDH）和谷胱甘肽S-转移酶（消费税）。链脲佐菌素诱发的实验性糖尿病大鼠的血糖，糖化血红蛋白以及血浆ALT和AST活性增加。长期高血糖症导致糖尿病动物的GSHPx（降低26％），过氧化氢酶（降低34％），GST（降低38％）和G6PDH（降低27％）的活性。我们没有观察到肝中膜脂质过氧化产物的积累增加或谷胱甘肽还原水平的改变。 ASA处理后，糖尿病动物中血糖和糖化血红蛋白之间的线性相关性发生了扭曲，这可能是由于非酶蛋白糖基化和蛋白乙酰化之间的化学竞争所致。 ASA的长期给药可以部分逆转GSHPx活性的降低，但不影响糖尿病大鼠中过氧化氢酶和GST的活性。否则，在ASA治疗的非糖尿病动物中注意到这些参数有所降低。在糖尿病和非糖尿病大鼠中均记录到ASA诱导的G6PDH活性增加。虽然由于糖尿病性高血糖引起的糖基化和ASA介导的乙酰化对除G6PDH以外的所有酶的活性都有非常相似的影响，但我们得出结论，葡萄糖或ASA的非酶修饰可能是观察到的趋同的常见机制。 （c）2006 Elsevier Inc.保留所有权利。

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