Schweinzer E, Waeg G, Esterbauer H, Goldenberg H
Department of Medical Chemistry, University of Vienna, Wien, Austria.
FEBS Lett. 1993 Nov 8;334(1):106-8. doi: 10.1016/0014-5793(93)81691-r.
We disprove that living cells stabilize ascorbate by the activity of a trans plasma membrane semidehydroascorbate reductase. The two processes show different specificities for both substrate and inhibitor. Not only cells but also cell-conditioned buffers stabilize ascorbate as long as compounds with molecular weights above 10 kDa are not removed. The effect is most probably due to chelation of traces of transition metals.
我们反驳了活细胞通过跨质膜半脱氢抗坏血酸还原酶的活性来稳定抗坏血酸这一观点。这两个过程对底物和抑制剂都表现出不同的特异性。只要分子量高于10 kDa的化合物未被去除,不仅细胞,而且细胞条件缓冲液都能稳定抗坏血酸。这种效应很可能是由于痕量过渡金属的螯合作用。