高血压和高胆固醇血症大鼠心肌黄嘌呤氧化还原酶活性。

Cardioscience Pub Date : 1993-03-01
M Janssen, J W de Jong, E Pasini, R Ferrari
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引用次数: 0

摘要

在一些物种中,黄嘌呤氧化还原酶活性似乎是心肌组织中自由基的主要来源。它的活性在发育和衰老过程中发生变化,至少在大鼠心脏中如此。几乎没有关于黄嘌呤氧化还原酶活性诱导自由基产生在高血压和高胆固醇血症这两种重要疾病中的活性的数据。因此,我们测定了自发性高血压心肌组织中黄嘌呤氧化酶和脱氢酶的活性。Wistar(控制高血压)、Yoshida(控制高胆固醇血症)和Brown Norway(控制高胆固醇血症)大鼠。细胞质组分在30℃,pH 8.3, 60微米黄嘌呤条件下孵育,用高效液相色谱法测定尿酸盐的形成。在Wistar组中,黄嘌呤氧化还原酶活性在衰老过程中相对稳定(约1.8 U/g蛋白)。高血压组18月时活性由1.7 U/g逐渐升高至2.3 U/g(与18月时Wistar比较p < 0.05)。在18个月时,两组的黄嘌呤氧化酶大约是两倍高(与2和6个月相比p < 0.001)。黄嘌呤脱氢酶和黄嘌呤氧化酶的比值在这个年龄下降了42% (p < 0.001)。在吉田组和布朗挪威组中,黄嘌呤氧化还原酶活性相似,在6个月时达到峰值。这些数据表明,高胆固醇血症状态不影响黄嘌呤氧化还原酶活性。相反,在肥大心肌中,黄嘌呤氧化还原酶活性高于对照组,表明自由基产生的潜力不同。(摘要删节250字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Myocardial xanthine oxidoreductase activity in hypertensive and hypercholesterolemic rats.

In several species, xanthine oxidoreductase activity seems to be a major source of free radicals in myocardial tissue. Its activity changes during development and aging, at least in the rat heart. Hardly any data are available about its activity in two important diseases, hypertension and hypercholesterolemia, in which the production of free radicals induced by xanthine oxidoreductase activity could play a role. Therefore we measured the activity of xanthine oxidase and dehydrogenase in myocardial tissue of spontaneously hypertensive. Wistar (control hypertensive), Yoshida (hypercholesterolemic) and Brown Norway (control hypercholesterolemic) rats of various ages. Cytosolic fractions were incubated at 30 degrees C, pH 8.3, with 60 microM xanthine, and the formation of urate was measured with high performance liquid chromatography. In the Wistar group, xanthine oxidoreductase activity was relatively constant during aging (about 1.8 U/g protein). In the hypertensive group, the activity increased gradually from 1.7 to 2.3 U/g at 18 months (p < 0.05 compared with Wistar at 18 months). Xanthine oxidase was about twice as high in both groups at 18 months (p < 0.001 compared with 2 and 6 months). The ratio of xanthine dehydrogenase to xanthine oxidase had decreased 42% at this age (p < 0.001). In the Yoshida and Brown Norway groups, xanthine oxidoreductase activity was similar, with a peak at 6 months. These data suggest that the hypercholesterolemic state does not influence xanthine oxidoreductase activity. In contrast, in hypertrophied myocardium, xanthine oxidoreductase activity was higher than in the control, suggesting a different potential for free-radical generation.(ABSTRACT TRUNCATED AT 250 WORDS)

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