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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Relationship between (Na plus K)-ATPase activity, lipid peroxidation and fatty acid profile in erythrocytes of hypertensive and normotensive subjects
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Relationship between (Na plus K)-ATPase activity, lipid peroxidation and fatty acid profile in erythrocytes of hypertensive and normotensive subjects

机译:高血压和血压正常个体红细胞中(Na + K)-ATPase活性,脂质过氧化与脂肪酸谱的关系

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Oxidative stress may play a role in the pathogenic mechanism of essential hypertension. Lipid peroxidation can alter the cellular structure of membrane-bound enzymes by changing the membrane phospholipids fatty acids composition. We investigated the relationship between (Na + K)-ATPase activity, lipid peroxidation, and erythrocyte fatty acid composition in essential hypertension. The study included 40 essential hypertensive and 49 healthy normotensive men (ages 35-60 years). Exclusion criteria were obesity, dyslipidemia, diabetes mellitus, smoking, and any current medication. Patients underwent 24-h ambulatory blood pressure monitoring and blood sampling. Lipid peroxidation was measured in the plasma and erythrocytes as 8-isoprostane or malondialdehyde (MDA), respectively. Antioxidant capacity was measured as ferric reducing ability of plasma (FRAP) in the plasma and as reduced/oxidized glutathione (GSH/GSSG ratio) in erythrocytes. (Na + K)-ATPase activity and fatty acids were determined in erythrocyte membranes. Hypertensives had higher levels of plasma 8-isoprostane, erythrocyte MDA, and relative percentage of saturated membrane fatty acids, but lower plasma FRAP levels, erythrocyte GSH/GSSG ratio, (Na + K)-ATPase activity and relative percentage of unsaturated membrane fatty acids, compared with normotensives. Day-time systolic and diastolic blood pressures correlated positively with lipid peroxidation parameters, but negatively with (Na + K)-ATPase activity. These findings suggest that the modulation of (Na + K)-ATPase activity may be associated with changes in the fatty acid composition induced by oxidative stress and provide evidence of a role for this enzyme in the pathophysiology of essential hypertension.
机译:氧化应激可能在原发性高血压的发病机制中起作用。脂质过氧化可通过改变膜磷脂脂肪酸组成来改变膜结合酶的细胞结构。我们调查了原发性高血压中(Na + K)-ATPase活性,脂质过氧化和红细胞脂肪酸组成之间的关系。该研究包括40名原发性高血压和49名健康的正常血压男性(年龄35-60岁)。排除标准为肥胖,血脂异常,糖尿病,吸烟和任何现有药物。患者接受24小时动态血压监测和血液采样。血浆和红细胞中的脂质过氧化分别以8-异前列腺素或丙二醛(MDA)的形式测量。测量抗氧化剂的能力,作为血浆中血浆的铁还原能力(FRAP)和红细胞中还原/氧化的谷胱甘肽(GSH / GSSG比)。测定了红细胞膜中的(Na + K)-ATPase活性和脂肪酸。高血压患者的血浆8-异前列腺素,红细胞MDA和饱和膜脂肪酸的相对百分比水平较高,但血浆FRAP水平,红细胞的GSH / GSSG比,(Na + K)-ATPase活性和不饱和膜脂肪酸的相对百分比较低,与血压正常者相比。白天的收缩压和舒张压与脂质过氧化参数呈正相关,而与(Na + K)-ATPase活性呈负相关。这些发现表明,(Na + K)-ATPase活性的调节可能与氧化应激诱导的脂肪酸组成的变化有关,并提供了该酶在原发性高血压的病理生理中的作用的证据。

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