Grummt F, Weinmann-Dorsch C, Schneider-Schaulies J, Lux A
Exp Cell Res. 1986 Mar;163(1):191-200. doi: 10.1016/0014-4827(86)90572-0.
DNA synthesis and adenosine(5')tetraphosphate(5')adenosine (Ap4A) levels decrease in cells treated with EDTA. The inhibitory effect of EDTA can be reversed with micromolar amounts of ZnCl2. ZnCl2 in micromolar concentrations also inhibits Ap4A hydrolase and stimulates amino acid-dependent Ap4A synthesis, suggesting that Zn2+ is modulating intracellular Ap4A pools. Serum addition to G1-arrested cells enhances uptake of Zn, whereas serum depletion leads to a fivefold decrease of the rates of zinc uptake. These results are discussed by regarding Zn2+ as a putative 'second messenger' of mitogenic induction and Ap4A as a possible 'third messenger' and trigger of DNA synthesis.
用乙二胺四乙酸(EDTA)处理的细胞中,DNA合成及腺苷-5'-四磷酸-5'-腺苷(Ap4A)水平降低。乙二胺四乙酸(EDTA)的抑制作用可用微摩尔量的氯化锌(ZnCl2)逆转。微摩尔浓度的氯化锌(ZnCl2)也会抑制Ap4A水解酶,并刺激氨基酸依赖性Ap4A合成,这表明锌离子(Zn2+)正在调节细胞内Ap4A库。向处于G1期停滞的细胞中添加血清可增强锌的摄取,而血清缺乏则导致锌摄取速率降低五倍。通过将锌离子(Zn2+)视为有丝分裂诱导的假定“第二信使”,以及将Ap4A视为可能的“第三信使”和DNA合成触发因素,对这些结果进行了讨论。