Forsbeck K, Bjelkenkrantz K, Nilsson K
Scand J Haematol. 1986 Nov;37(5):429-37. doi: 10.1111/j.1600-0609.1986.tb02633.x.
Suramin was used to analyze the growth-effects of blockade of iron uptake on two established human cell lines, U-937 (monocytoid) and K-562 (erythroleukemic). Suramin suppressed cell surface transferrin (Tf) binding and uptake of iron via inhibition of receptor-mediated endocytosis (RME). As a result, both lines accumulated in the S-phase. DNA synthesis and cell division were inhibited in the suramin-treated U-937, but not in K-562. Iron, supplied by a route alternative to Tf-to suramin-suppressed U-937 cells, reinitiated DNA synthesis and cell division, although at a lower level than in control cells. Multiple effects on iron-dependent enzymes and an inhibition of binding of undefined growth factors necessary for the transition through the cell cycle are suggested to be mechanisms by which suramin affects the U-937 cells. The results imply that clinically observed side effects of suramin may be caused by interference with cellular iron metabolism.
苏拉明用于分析阻断铁摄取对两种已建立的人类细胞系U - 937（单核细胞样）和K - 562（红白血病）生长的影响。苏拉明通过抑制受体介导的内吞作用（RME）来抑制细胞表面转铁蛋白（Tf）的结合以及铁的摄取。结果，这两种细胞系都停滞在S期。在经苏拉明处理的U - 937细胞中，DNA合成和细胞分裂受到抑制，但在K - 562细胞中未受抑制。通过一种替代转铁蛋白的途径向经苏拉明处理的U - 937细胞提供铁，可重新启动DNA合成和细胞分裂，尽管其水平低于对照细胞。对铁依赖性酶的多种影响以及对细胞周期转换所必需的未定义生长因子结合的抑制作用被认为是苏拉明影响U - 937细胞的机制。结果表明，临床上观察到的苏拉明副作用可能是由对细胞铁代谢的干扰引起的。
