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Estrogen, neutrophils and oxidation

机译:雌激素,中性粒细胞与氧化

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The potential role of estrogens in the prevention of cardiovascular disease (CVD) is still under debate. Previous studies from our laboratory have shown that estradiol may act as a pro oxidant at physiological concentrations, enhancing peroxidase-mediated oxidation of low density lipoprotein (LDL). In the present study, we show that physiological concentrations of estradiol enhance fMLP-mediated neutrophil degranulation and oxidative stress markers. For example, 10 nM estradiol increased myeloperoxidase (MPO), elastase, and superoxide release by 19.9 +/- 9.6% (p = 0.006), 16.3 +/- 5.2% (p = 0.09), and 36.1 +/- 19.5% (p = 0.05), respectively. The enhancement of neutrophil degranulation by estradiol resulted in an increase in the formation of LDL oxidation markers such as conjugated dienes and thiobarbituric acid-reactive substances (20.7 +/- 7.2%, p = 0.04). Thus, estradiol can act as a pro oxidant, promoting neutrophil degranulation as well as reacting with MPO to enhance the oxidation of LDL. This mechanism supports our hypothesis that oxidative stress may be beneficial towards the prevention of CVD both by promoting plasma oxidation of LDL, with its subsequent clearance by the liver, as well as by inducing a threshold antioxidant defense in the arteries. Our study also suggests that estradiol by promoting oxidation in the plasma is beneficial in preventing CVD. (C) 2004 Elsevier Inc. All rights reserved.
机译:雌激素在预防心血管疾病(CVD)中的潜在作用仍在争论中。我们实验室的先前研究表明,雌二醇在生理浓度下可能充当促氧化剂,从而增强了过氧化物酶介导的低密度脂蛋白(LDL)的氧化。在本研究中,我们显示了雌二醇的生理浓度可增强fMLP介导的中性粒细胞脱粒和氧化应激标志物。例如,10 nM雌二醇使髓过氧化物酶(MPO),弹性蛋白酶和超氧化物的释放增加19.9 +/- 9.6%(p = 0.006),16.3 +/- 5.2%(p = 0.09)和36.1 +/- 19.5%( p = 0.05)。雌二醇增强中性粒细胞脱粒的作用导致LDL氧化标记物(如共轭二烯和硫代巴比妥酸反应性物质)的形成增加(20.7 +/- 7.2%,p = 0.04)。因此,雌二醇可以充当促氧化剂,促进中性粒细胞脱粒以及与MPO反应以增强LDL的氧化。这种机制支持了我们的假设,即氧化应激可能通过促进LDL的血浆氧化,随后被肝脏清除以及通过诱导动脉中的抗氧化剂防御作用而对预防CVD有益。我们的研究还表明,雌二醇可通过促进血浆中的氧化来预防CVD。 (C)2004 Elsevier Inc.保留所有权利。

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