高半胱氨酸还原脱氢抗坏血酸。,Biochimica et Biophysica Acta (BBA) - General Subjects

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高半胱氨酸还原脱氢抗坏血酸。
Biochimica et Biophysica Acta (BBA) - General Subjects ( IF 2.8 ) Pub Date : 2001-05-09 , DOI: 10.1016/s0304-4165(00)00186-0
J B Park ₁

Affiliation

为了确定细胞外脱氢抗坏血酸（DHA）的还原过程，测试了分子（同型半胱氨酸，高半胱氨酸硫代内酯，蛋氨酸，半胱氨酸和高丝氨酸），以鉴定具有将DHA还原为抗坏血酸（AA）潜力的分子。同型半胱氨酸（Hcy）是最有效的测试分子。将Hcy的功效与其他能够降低DHA的分子（还原型谷胱甘肽（GSH）和半胱氨酸（Cy））的功效进行了比较。尽管所有三个分子均能够还原DHA，但GSH和Cy在低于100 micromol / l的浓度下无法将DHA还原为AA，而在200-300 micromol / l的浓度下只有不到5％的DHA被还原为AA。相反，Hcy在低至10 micromol / l的浓度下将DHA化学计量地还原为AA。在Jurkat和U937细胞中，细胞外Hcy浓度的增加抑制了细胞内脱氢抗坏血酸的摄取，表明细胞内Hcy降低DHA导致细胞外DHA可用于其细胞内摄取。在槲皮素（一种DHA摄取抑制剂）的存在下，细胞外Hcy和DHA的同时氧化和还原被加速，这表明细胞外抗坏血酸的浓度通过抑制槲皮素摄取DHA和通过Hcy减少细胞外DHA而增加。用人脐静脉内皮细胞证实了同型半胱氨酸对DHA减少和摄取的影响。Hcy的氧化作用还阻止了人脐静脉内皮细胞DNA合成的减少，这种减少会在暴露于Hcy后发生。这表明Hcy引起的细胞外DHA减少导致细胞内DHA可用于其细胞内摄取的减少。在槲皮素（一种DHA摄取抑制剂）的存在下，细胞外Hcy和DHA的同时氧化和还原被加速，这表明细胞外抗坏血酸的浓度通过抑制槲皮素摄取DHA和通过Hcy减少细胞外DHA而增加。人脐静脉内皮细胞证实了同型半胱氨酸对DHA减少和摄取的影响。Hcy的氧化作用还阻止了人脐静脉内皮细胞DNA合成的减少，这种减少会在暴露于Hcy后发生。这表明Hcy引起的细胞外DHA减少导致细胞内DHA可用于其细胞内摄取的减少。在槲皮素（一种DHA摄取抑制剂）的存在下，细胞外Hcy和DHA的同时氧化和还原被加速，这表明细胞外抗坏血酸的浓度通过抑制槲皮素摄取DHA和通过Hcy减少细胞外DHA而增加。人脐静脉内皮细胞证实了同型半胱氨酸对DHA减少和摄取的影响。Hcy的氧化作用还阻止了人脐静脉内皮细胞DNA合成的减少，这种减少会在暴露于Hcy后发生。在槲皮素（一种DHA摄取抑制剂）的存在下，细胞外Hcy和DHA的同时氧化和还原被加速，这表明细胞外抗坏血酸的浓度通过抑制槲皮素摄取DHA和通过Hcy减少细胞外DHA而增加。人脐静脉内皮细胞证实了同型半胱氨酸对DHA减少和摄取的影响。Hcy的氧化作用还阻止了人脐静脉内皮细胞DNA合成的减少，这种减少会在暴露于Hcy后发生。在槲皮素（一种DHA摄取抑制剂）的存在下，细胞外Hcy和DHA的同时氧化和还原被加速，这表明细胞外抗坏血酸的浓度通过抑制槲皮素摄取DHA和通过Hcy减少细胞外DHA而增加。用人脐静脉内皮细胞证实了同型半胱氨酸对DHA减少和摄取的影响。Hcy的氧化作用还阻止了人脐静脉内皮细胞DNA合成的减少，这种减少会在暴露于Hcy后发生。人脐静脉内皮细胞证实了同型半胱氨酸对DHA减少和摄取的影响。Hcy的氧化作用还阻止了人脐静脉内皮细胞DNA合成的减少，这种减少会在暴露于Hcy后发生。人脐静脉内皮细胞证实了同型半胱氨酸对DHA减少和摄取的影响。Hcy的氧化作用还阻止了人脐静脉内皮细胞DNA合成的减少，这种减少会在暴露于Hcy后发生。

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Reduction of dehydroascorbic acid by homocysteine.

To determine the reductive process of extracellular dehydroascorbic acid (DHA), molecules (homocysteine, homocysteine thiolactone, methionine, cysteine, and homoserine) were tested to identify those with the potential to reduce DHA to ascorbic acid (AA). Homocysteine (Hcy) was the most potent of the molecules tested. The efficacy of Hcy was compared with that of other molecules able to reduce DHA (reduced glutathione (GSH) and cysteine (Cy)). Although all three molecules were able to reduce DHA, GSH and Cy were not to reduce DHA to AA at concentrations lower than 100 micromol/l, and only less than 5% DHA was reduced to AA at concentrations of 200-300 micromol/l. In contrast, Hcy reduced DHA to AA stoichiometrically at concentrations as low as 10 micromol/l. In Jurkat and U937 cells, the increasing concentrations of extracellular Hcy suppressed intracellular dehydroascorbic acid uptake, indicating that extracellular reduction of DHA by Hcy leads to decreasing extracellular DHA available for its intracellular uptake. Simultaneous oxidation and reduction of Hcy and DHA were accelerated extracellularly in the presence of quercetin, an inhibitor of DHA uptake, suggesting that extracellular ascorbic acid concentration increased via blocking DHA uptake by quercetin and reducing extracellular DHA by Hcy. The effect of homocysteine on DHA reduction and uptake was confirmed with human umbilical vein endothelial cells. The oxidation of Hcy also prevented the decrease in DNA synthesis in human umbilical vein endothelial cells, which would occur following exposure to Hcy.

更新日期：2019-11-01

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