Ricetti M M, Guidi G C, Bellisola G, Marrocchella R, Rigo A, Perona G
Cattedra di Ematologia, Valeggio s.M. Università di Verona, Italy.
Biol Trace Elem Res. 1994 Oct-Nov;46(1-2):113-23. doi: 10.1007/BF02790072.
Selenium (Se) is an essential component of glutathione peroxidase (GSH-Px), an enzyme that protects cells by reducing intracellular peroxides. Impaired Se status and GSH-Px activity seem associated with increased risk of atherosclerotic vascular diseases. This study reports the effects of Se supplementation on GSH-Px activity, on prostacyclin (PGI2) production, on 12-hydroxy-eicosatetraenoic acid (12-HETE) levels, and on GSH-Px mRNA expression in cultured human umbilical vein endothelial cells (HUVEC). Se-enriched HUVEC showed significant increase of both GSH-Px activity and thrombin-stimulated production of PGI2 in the presence of stable concentrations of 12-HETE. On the other hand, an inverse correlation between Se concentrations in culture media and GSH-Px mRNA levels in Northern blot analysis was shown; this suggests that a major degree of regulation for GSH-Px expression by Se is most likely exerted at the posttranscriptional level. These observations may help to explain the increased incidence of atherosclerosis described in Se-deficient individuals.
硒(Se)是谷胱甘肽过氧化物酶(GSH-Px)的重要组成部分,该酶通过还原细胞内过氧化物来保护细胞。硒状态受损和GSH-Px活性似乎与动脉粥样硬化性血管疾病风险增加有关。本研究报告了补充硒对培养的人脐静脉内皮细胞(HUVEC)中GSH-Px活性、前列环素(PGI2)生成、12-羟基二十碳四烯酸(12-HETE)水平以及GSH-Px mRNA表达的影响。在稳定浓度的12-HETE存在下,富硒的HUVEC显示出GSH-Px活性和凝血酶刺激的PGI2生成均显著增加。另一方面,在Northern印迹分析中显示培养基中的硒浓度与GSH-Px mRNA水平呈负相关;这表明硒对GSH-Px表达的主要调节程度很可能在转录后水平发挥作用。这些观察结果可能有助于解释缺硒个体中动脉粥样硬化发病率增加的现象。