Patierno S R, Costa M
Chem Biol Interact. 1985 Oct;55(1-2):75-91. doi: 10.1016/s0009-2797(85)80121-6.
The carcinogenic activity of crystalline NiS has been attributed to phagocytosis and intracellular dissolution of the particles to yield Ni2+ which is thought to enter the nucleus and damage DNA. In this study the extent and type of DNA damage in Chinese hamster ovary CHO cells treated with various nickel compounds was assessed by alkaline elution. Both insoluble (crystalline NiS) and soluble (NiCl2) nickel compounds induced single strand breaks and DNA protein cross-links. The single strand breaks were repaired relatively quickly but the DNA-protein cross-links were present and still accumulating 24 h after exposure to nickel. Single strand breakage occurred at both non-cytotoxic and cytotoxic concentrations of nickel, however, DNA-protein cross-linking was absent when cells were exposed to toxic nickel levels. The concentration of nickel that induced DNA-protein cross-linking correlated with those metal concentrations that reversibly inhibited cellular replication.
结晶态硫化镍的致癌活性被认为是由于颗粒被吞噬并在细胞内溶解产生Ni2+，而Ni2+被认为会进入细胞核并损伤DNA。在本研究中，通过碱性洗脱评估了用各种镍化合物处理的中国仓鼠卵巢（CHO）细胞中DNA损伤的程度和类型。不溶性（结晶态硫化镍）和可溶性（氯化镍）镍化合物均能诱导单链断裂和DNA-蛋白质交联。单链断裂能较快修复，但DNA-蛋白质交联在接触镍24小时后仍存在且不断积累。镍在非细胞毒性和细胞毒性浓度下均会导致单链断裂，然而，当细胞暴露于毒性镍水平时，不存在DNA-蛋白质交联。诱导DNA-蛋白质交联的镍浓度与可逆抑制细胞复制的金属浓度相关。
