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首页> 外文期刊>Protoplasma: An International Journal of Cell Biology >MECHANISMS OF VITAMIN C STABILIZATION BY K562 ERYTHROLEUKEMIC CELLS
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MECHANISMS OF VITAMIN C STABILIZATION BY K562 ERYTHROLEUKEMIC CELLS

机译:K562红白血病细胞对维生素C的稳定作用机理

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K562 cells display several possibilities to keep ascorbic acid in the surrounding medium in the reduced state and prevent its loss by degradation of the oxidized form, dehydroascorbic acid: (1) A semidehydroascorbic acid reductase with high affinity for the ascorbate radical scavenges this before it disproportionates into the two parent forms of vitamin C (ascorbate and dehydroascorbic acid). (2) Dehydroascorbic acid in the extracellular medium is slowly converted to ascorbate by a different mechanism with low affinity which may or may not involve uptake of the oxidized and release of the reduced form. (3) Ascorbate remains relatively stable in the cell culture medium in presence, but also in absence of the cells after their removal. This is most probably due to the presence of released peptides in the cell-conditioned medium which can chelate transition metal ions and thus prevent catalytic autoxidation of ascorbate. [References: 40]
机译:K562细胞显示出多种可能性,可将抗坏血酸保持在还原状态,并通过氧化形式脱氢抗坏血酸的降解防止其丢失:(1)对抗坏血酸自由基具有高亲和力的半脱氢抗坏血酸还原酶可在其歧化之前对其进行清除。分为两种母体形式的维生素C(抗坏血酸和脱氢抗坏血酸)。 (2)细胞外培养基中的脱氢抗坏血酸通过不同的机制以低亲和力缓慢转化为抗坏血酸,该亲和力可能会或可能不会吸收氧化并释放还原形式。 (3)抗坏血酸盐在存在时在细胞培养基中保持相对稳定,但在去除细胞后不存在细胞时也保持相对稳定。这很可能是由于细胞条件培养基中存在释放的肽,该肽会螯合过渡金属离子,从而阻止抗坏血酸的催化自氧化。 [参考:40]

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