Vatan Özgür
Department of Biology, Faculty of Arts and Science, Görükle Campus, Bursa Uludağ University, 16059 Nilüfer, Bursa, Turkey.
Toxics. 2022 Aug 24;10(9):492. doi: 10.3390/toxics10090492.
The use of iron-nickel alloy nanoparticles (Fe-Ni ANPs) is increasing daily in various fields. People are increasingly exposed to these nanoparticles for occupational and environmental reasons. Our study determined some of the effects of Fe-Ni ANP exposure and impacts on human health at the cellular level. The cytotoxic and genotoxic potentials of Fe-Ni ANPs were investigated by XTT, clonogenic, comet, and GammaH2AX analyses using Beas-2B cells. Annexin V, multicaspase, and cell cycle arrest methods were used to understand the apoptotic mechanism of action. The intracellular ROS method was used to determine the primary mechanism that leads to cytotoxic and genotoxic activity. The Fe-Ni ANPs showed cytotoxic activity with the XTT and clonogenic methods: they had genotoxic potential, as demonstrated via genotoxicity methods. It was determined that the cytotoxic effect was realized by the caspase-dependent apoptotic pathway, and the cells were stopped at the G0/G1 stage by Fe-Ni ANPs. Increased intracellular ROS due to Fe-Ni ANPs led to cytotoxic, genotoxic, and apoptotic activity. Potential risks to human health due to Fe-Ni ANPs were then demonstrated at the cellular level.
铁镍合金纳米颗粒（Fe-Ni ANPs）在各个领域的应用日益广泛。由于职业和环境原因，人们越来越多地接触到这些纳米颗粒。我们的研究确定了Fe-Ni ANP暴露在细胞水平上对人体健康的一些影响。使用Beas-2B细胞，通过XTT、克隆形成、彗星试验和GammaH2AX分析研究了Fe-Ni ANPs的细胞毒性和遗传毒性潜力。采用膜联蛋白V、多胱天蛋白酶和细胞周期阻滞方法来了解其凋亡作用机制。通过细胞内活性氧方法确定导致细胞毒性和遗传毒性活性的主要机制。Fe-Ni ANPs通过XTT和克隆形成方法表现出细胞毒性活性：通过遗传毒性方法证明它们具有遗传毒性潜力。确定细胞毒性作用是通过半胱天冬酶依赖性凋亡途径实现的，并且Fe-Ni ANPs使细胞停滞在G0/G1期。Fe-Ni ANPs导致的细胞内活性氧增加导致细胞毒性、遗传毒性和凋亡活性。随后在细胞水平上证明了Fe-Ni ANPs对人体健康的潜在风险。
