Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Bucharest, 91-95 Splaiul Independentei, 050095 Bucharest, Romania.
Research Institute of the University of Bucharest-ICUB, University of Bucharest, 050657 Bucharest, Romania.
Int J Mol Sci. 2023 Mar 29;24(7):6401. doi: 10.3390/ijms24076401.
The current study was focused on the potential of pure P25 TiO nanoparticles (NPs) and Fe(1%)-N co-doped P25 TiO NPs to induce cyto- and genotoxic effects in MRC-5 human pulmonary fibroblasts. The oxidative lesions of P25 NPs were reflected in the amount of 8-hydroxydeoxyguanosine accumulated in DNA and the lysosomal damage produced, but iron-doping partially suppressed these effects. However, neither P25 nor Fe(1%)-N co-doped P25 NPs had such a serious effect of inducing DNA fragmentation or activating apoptosis signaling. Moreover, oxo-guanine glycosylase 1/2, a key enzyme of the base excision repair mechanism, was overexpressed in response to the oxidative DNA deterioration induced by P25 and P25-Fe(1%)-N NPs.
本研究旨在探讨纯 P25 TiO 纳米粒子（NPs）和 Fe(1%)-N 共掺杂 P25 TiO NPs 是否具有诱导 MRC-5 人肺成纤维细胞细胞毒性和遗传毒性的潜力。P25 NPs 的氧化损伤反映在 DNA 中积累的 8-羟基脱氧鸟苷的量和产生的溶酶体损伤上，但铁掺杂部分抑制了这些效应。然而，P25 和 Fe(1%)-N 共掺杂 P25 NPs 都没有严重到诱导 DNA 片段化或激活凋亡信号的程度。此外，氧化 DNA 损伤诱导 P25 和 P25-Fe(1%)-N NPs 上调碱基切除修复机制中的关键酶——氧鸟嘌呤糖苷酶 1/2 的表达。
