Skreb Y, Fischer A B
Zentralbl Bakteriol Mikrobiol Hyg B. 1984 Jan;178(5-6):432-45.
The effects of nickel chloride were studied in two human cell lines, HeLa and diploid embryonic fibroblasts, as well as in V79 Chinese hamster cells and in L-A mouse fibroblasts. NiCl2 produces a dose-dependent depression of proliferation and mitotic rate. Effects on viability are accompanied by an increasing release of the intracellular enzyme lactic dehydrogenase. Lactic acid production is stimulated. The plating efficiency is reduced, as are DNA and protein synthesis and, to a lesser degree, RNA synthesis. Comparing these results with those of previous studies of the cytotoxicity of other heavy metals in the same test systems, similar effects are observed though with different intensities and slight differences between the cell lines employed. As regards lethal effects (LC50) the following rank order of cytotoxicity can be established: Ni2+ approximately equal to Pb2+ less than Mn2+ less than Hg2+ less than Cd2+; as regards growth inhibition the same rank order is observed as in the case of the LC50 in HeLa and human fibroblasts, but in L-A cells Ni2+ is more inhibitive than the other metal ions listed above with the exception of Cd2+. With respect to colony formation NiCl2 is less effective than PbCl2, MnCl2, and CdCl2. NiCl2 effects in serum-free medium are much faster and more severe than in medium containing serum or serum albumin indicating that serum constituents, notably albumin, bind the metal effectively and inhibit cellular uptake; this confirms reports of other authors on the serum binding and slow uptake of NiCl2. Synchronized cells are most sensitive in the G1 and early S phases of the cell cycle. Together with the finding that thymidine incorporation is affected to a considerable degree this contributes an explanation of the known genotoxic effects of nickel.
在两种人类细胞系（HeLa细胞和二倍体胚胎成纤维细胞）以及V79中国仓鼠细胞和L - A小鼠成纤维细胞中研究了氯化镍的作用。NiCl₂可产生剂量依赖性的增殖和有丝分裂率抑制。对细胞活力的影响伴随着细胞内乳酸脱氢酶释放的增加。乳酸生成受到刺激。平板接种效率降低，DNA和蛋白质合成以及在较小程度上RNA合成也降低。将这些结果与之前在相同测试系统中对其他重金属细胞毒性的研究结果进行比较，观察到了相似的效应，尽管强度不同且所用细胞系之间存在细微差异。关于致死效应（LC50），可确定以下细胞毒性的排序：Ni²⁺约等于Pb²⁺ ＜ Mn²⁺ ＜ Hg²⁺ ＜ Cd²⁺；关于生长抑制，在HeLa细胞和人类成纤维细胞中观察到与LC50情况相同的排序，但在L - A细胞中，除了Cd²⁺外，Ni²⁺比上述其他金属离子更具抑制性。关于集落形成，NiCl₂的效果比PbCl₂、MnCl₂和CdCl₂差。NiCl₂在无血清培养基中的作用比在含有血清或血清白蛋白的培养基中更快且更严重，这表明血清成分，尤其是白蛋白，能有效结合金属并抑制细胞摄取；这证实了其他作者关于NiCl₂血清结合和缓慢摄取的报道。同步化细胞在细胞周期的G1期和早期S期最敏感。连同胸苷掺入受到相当程度影响这一发现，这有助于解释镍已知的遗传毒性作用。
