[Fe(NO)₂] – modified nanoparticles of low-density protein (DNICLDL) can serve as conveyors of iron in the form of stable complexes with ApoB100 protein. As reported recently, in human hepatoma cells DNICLDL significantly increased the total iron content, while showing low toxicity. In the present work, we focused on the effects of internalization of DNIC-modified lipoproteins in macrophages, with special regards to cytotoxicity. DNICLDL was administered to a model macrophage cell line, RAW 264.7. Administration of DNICLDL considerably increased total iron content. High increase of iron was accompanied by moderate toxicity. As shown by in vitro plasmid nicking assay, chelation of iron in the form of DNIC strongly reduced the iron-related reactive oxygen species (ROS) -induced DNA damage. In addition, DNICLDL, plausibly due to its NO-donating activity, did not induce inducible nitric oxide synthase (iNOS) expression, as opposed to other forms of low-density protein (LDL).

[Fe（NO）₂] –低密度蛋白质（DNICLDL）的修饰纳米粒子可以与ApoB100蛋白质形成稳定的复合物形式，作为铁的输送剂。如最近报道，在人肝癌细胞中，DNICLDL显着增加了总铁含量，同时显示出低毒性。在当前的工作中，我们着重研究了DNIC修饰的脂蛋白在巨噬细胞中的内在化作用，并特别考虑了细胞毒性。将DNICLDL施用于模型巨噬细胞系RAW 264.7。DNICLDL的使用大大增加了总铁含量。铁的大量增加伴有中度毒性。如体外质粒切口测定所示，DNIC形式的铁螯合强烈地减少了铁相关的活性氧（ROS）诱导的DNA损伤。此外，DNICLDL可能是由于其捐赠NO的活性，