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人体红细胞针对吸烟的抗氧化防御反应——谷胱甘肽 S-转移酶易感性

Erythrocyte antioxidant defense response against cigarette smoking in humans--the glutathione S-transferase vulnerability.

作者信息

Orhan Hilmi, Evelo Chris T A, Sahin Gönül

机构信息

Department of Toxicology, Faculty of Pharmacy, Hacettepe University, 06100 Ankara, Turkey.

出版信息

J Biochem Mol Toxicol. 2005;19(4):226-33. doi: 10.1002/jbt.20088.

Abstract

Cigarette smoking leads to uptake of a multitude of reactive chemicals including many electrophiles and may also give rise to oxidative stress. Human red blood cells are important targets for electrophilic and oxidant foreign compounds. We investigated the oxidative stress in erythrocytes upon cigarette smoking, and the response of antioxidant defense system against it. With this aim, simultaneous determination of erythrocyte superoxide dismutase (SOD), selenium dependent glutathione peroxidase (Se-GPx), catalase (CAT), glutathione S-transferase (GST) activities and plasma levels of thiobarbituric acid reactive substances (TBARS), and the degree of erythrocyte membrane lipid peroxidation (EMLP) were carried out in blood samples of smokers and their controls. Plasma TBARS levels and EMLP in smokers were significantly higher than the control levels (p < 0.01 and p < 0.005, respectively). SOD activity was diminished in smokers compared to nonsmoker controls (p < 0.005). Erythrocyte Se-GPx activity was also found significantly diminished in smokers (p < 0.005), while plasma Se-GPx activity was not changed. We observed that erythrocyte CAT activity was not different in smokers compared to nonsmoker controls. We found that the erythrocyte GST activity is significantly lower in young adult smokers (3.03 +/- 0.18 U/mg protein; mean +/- SEM; n = 46) than in nonsmoking contemporaries (3.98 +/- 0.26 U/mg protein; mean +/- SEM; n = 41). Together with previously reported data, it can be concluded that the decrease in GST activity leads to extra GST synthesis during erythrocyte proliferation. The same data were also analyzed for the sex differences. The statistically significant differences remained the same between nonsmoker and smoker females. Only EMLP degree and SOD activity were significantly different between nonsmoker and smoker males; however, when compared the parameters between male and female nonsmokers, GST activity was found to be significantly higher in females than that of males.

摘要

吸烟会导致人体摄入多种活性化学物质,其中包括许多亲电试剂,还可能引发氧化应激。人类红细胞是亲电和氧化性外来化合物的重要作用靶点。我们研究了吸烟对红细胞氧化应激的影响,以及抗氧化防御系统对此的反应。为此,我们同时测定了吸烟者及其对照者血液样本中红细胞超氧化物歧化酶(SOD)、硒依赖性谷胱甘肽过氧化物酶(Se-GPx)、过氧化氢酶(CAT)、谷胱甘肽S-转移酶(GST)的活性以及血浆中硫代巴比妥酸反应性物质(TBARS)的水平,以及红细胞膜脂质过氧化程度(EMLP)。吸烟者的血浆TBARS水平和EMLP显著高于对照水平(分别为p < 0.01和p < 0.005)。与不吸烟的对照者相比,吸烟者的SOD活性降低(p < 0.005)。还发现吸烟者红细胞Se-GPx活性显著降低(p < 0.005),而血浆Se-GPx活性未发生变化。我们观察到,与不吸烟的对照者相比,吸烟者的红细胞CAT活性没有差异。我们发现,年轻成年吸烟者(3.03 +/- 0.18 U/mg蛋白质;平均值 +/- 标准误;n = 46)的红细胞GST活性显著低于同龄不吸烟者(3.98 +/- 0.26 U/mg蛋白质;平均值 +/- 标准误;n = 41)。结合先前报道的数据,可以得出结论,GST活性降低会导致红细胞增殖过程中额外的GST合成。我们还对这些数据进行了性别差异分析。不吸烟和吸烟女性之间的统计学显著差异保持不变。不吸烟和吸烟男性之间只有EMLP程度和SOD活性存在显著差异;然而,比较不吸烟男性和女性的参数时,发现女性的GST活性显著高于男性。

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