Löw H, Grebing C, Lindgren A, Tally M, Sun I L, Crane F L
Department of Endocrinology, Karolinska Institute, Stockholm, Sweden.
J Bioenerg Biomembr. 1987 Oct;19(5):535-49. doi: 10.1007/BF00770036.
Nonpermeable electron acceptors can be reduced by a transplasma membrane electron transport system in suspensions of intact cells. Here we report that diferric transferrin is reduced by HeLa S3 cells. The reduction is recorded spectrophotometrically as the formation of the ferrous complex of bathophenanthroline disulfonate. Ferric ammonium citrate can also be used as an electron acceptor and the presence of low concentrations of diferric transferrin greatly stimulates the reduction of trivalent iron under these conditions. Likewise very low concentrations of ferricyanide, which does not give rise to a ferrous bathophenanthroline disulfonate complex formation, have a strong stimulatory effect on the complex formation when ferric ammonium citrate is the source of ferric iron. Apotransferrin is a potent inhibitor of the reaction. The inhibition occurs at the concentration necessary for complete occupancy of the transferrin receptors. The inhibition can be demonstrated also when high concentrations of ferricyanide are used as electron acceptor. The possible mechanism behind the reported phenomena is discussed, and it is concluded that the transplasma membrane electron transport system can be involved in the process of cellular iron uptake.
非渗透性电子受体可被完整细胞悬液中的跨质膜电子传递系统还原。在此我们报告，HeLa S3细胞可还原二价铁转铁蛋白。通过分光光度法记录还原过程，即二磺酸邻二氮菲亚铁络合物的形成。柠檬酸铁铵也可用作电子受体，在这些条件下，低浓度二价铁转铁蛋白的存在极大地刺激了三价铁的还原。同样，极低浓度的铁氰化物（它不会形成二磺酸邻二氮菲亚铁络合物）在以柠檬酸铁铵作为铁源时，对络合物的形成有强烈的刺激作用。脱铁转铁蛋白是该反应的有效抑制剂。抑制作用发生在转铁蛋白受体完全被占据所需的浓度。当使用高浓度铁氰化物作为电子受体时，也能证明这种抑制作用。文中讨论了所报道现象背后可能的机制，并得出结论：跨质膜电子传递系统可能参与细胞铁摄取过程。
