Horvathova Martina, Zitnanova Ingrid, Kralovicova Zuzana, Balis Peter, Puzserova Angelika, Muchova Jana, Kluknavsky Michal, Durackova Zdenka, Bernatova Iveta
Institute of Medical Chemistry, Biochemistry and Clinical Biochemistry, Faculty of Medicine, Comenius University Bratislava, Slovak Republic.
Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Centre of Excellence for Examination of Regulatory Role of Nitric Oxide in Civilization Diseases, Bratislava, Slovak Republic.
Hypertens Res. 2016 Feb;39(2):64-9. doi: 10.1038/hr.2015.117. Epub 2015 Oct 29.
This study investigated the contribution of blood oxidative stress (OS) to the development of hypertension, as well as sex differences in the antioxidant defense system (ADS) in genetic models of hypertension. Nine-week-old normotensive Wistar-Kyoto (WKY) rats, borderline hypertensive rats (BHR) and spontaneously hypertensive rats (SHR) of both sexes were used. Systolic blood pressure (SBP) was determined by tail-cuff plethysmography, the trolox equivalent antioxidant capacity (TEAC) and the concentration of lipid peroxides (LP) were determined in plasma. The activity of the antioxidant enzymes Cu/Zn-superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) was determined in erythrocytes. SBP was significantly elevated in BHR and SHR in both sexes. BHR and SHR males had a higher SBP than the respective females. Sex-dependent differences in the ADS were found only in SHR, in which TEAC, SOD and CAT were significantly higher in males than in females. No differences in TEAC, SOD, CAT and GPx were observed between BHR (males and females) and WKY controls. LP levels were similar in all the groups investigated. Significant positive correlations were observed between SBP and both SOD and CAT. TEAC correlated positively with SOD and LP. As no signs of oxidative damage to lipids were found in young BHR and SHR of either sex, OS in the blood does not seem to be causatively related to the development of hypertension in these rats. However, despite activated antioxidant defenses, the positive correlation between plasma TEAC and LP suggests that oxidative damage is progressing slowly and therefore it seems to be a consequence rather than the cause of hypertension.
本研究调查了血液氧化应激（OS）在高血压发生发展中的作用，以及高血压遗传模型中抗氧化防御系统（ADS）的性别差异。使用了9周龄的正常血压Wistar-Kyoto（WKY）大鼠、临界高血压大鼠（BHR）和自发性高血压大鼠（SHR），雌雄皆有。通过尾套体积描记法测定收缩压（SBP），测定血浆中的Trolox等效抗氧化能力（TEAC）和脂质过氧化物（LP）浓度。测定红细胞中抗氧化酶铜/锌超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPx）和过氧化氢酶（CAT）的活性。BHR和SHR雌雄两性的SBP均显著升高。BHR和SHR雄性的SBP高于各自的雌性。仅在SHR中发现ADS存在性别依赖性差异，其中雄性的TEAC、SOD和CAT显著高于雌性。在BHR（雄性和雌性）与WKY对照组之间，未观察到TEAC、SOD、CAT和GPx的差异。所有研究组的LP水平相似。SBP与SOD和CAT均呈显著正相关。TEAC与SOD和LP呈正相关。由于在任何性别的年轻BHR和SHR中均未发现脂质氧化损伤的迹象，血液中的OS似乎与这些大鼠的高血压发生没有因果关系。然而，尽管抗氧化防御被激活，但血浆TEAC与LP之间的正相关表明氧化损伤正在缓慢进展，因此它似乎是高血压的结果而非原因。
