In recent years, the industrial use of ZnO quantum dots (QDs) and nanoparticles (NPs) has risen and there is a high chance of these nanoparticles affecting human health. In this study, different sizes of ZnO-NPs (6–100 nm) were prepared and characterized. The generation of reactive oxygen species (ROS) and its involvement in apoptosis when HepG2 cells were exposed to QDs (6 nm) and NPs of different sizes (15–20, 50, and 100 nm) was also investigated. At a concentration of 25–200 μg/mL, NPs induced dose-dependent cytotoxicity in HepG2 cells. The engineered NPs increased oxidative stress in a dose- and size-dependent manner, as seen by an increase in ROS production, lipid peroxidation, and glutathione reduction. Furthermore, cell-cycle analysis of HepG2 cells treated with different sizes of NPs showed an increase in the apoptotic peak after a 24-h exposure period. Quantitative real-time PCR data showed that the mRNA levels of apoptotic marker genes such as p53, bax, and caspase-3 were upregulated, whereas bcl-2, an anti-apoptotic gene, was downregulated; therefore, apoptosis was mediated through the p53, bax, caspase-3, and bcl-2 pathways, suggesting a possible mechanism by which QDs and NPs of ZnO mediate their toxicity.Graphic abstract

中文翻译：

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在人类细胞系中由工程纳米结构（量子点和纳米粒子）诱导的细胞毒性和细胞死亡。

近年来，ZnO 量子点 (QD) 和纳米粒子 (NP) 的工业应用有所增加，这些纳米粒子很有可能影响人类健康。在本研究中，制备并表征了不同尺寸的 ZnO-NPs（6-100 nm）。还研究了当 HepG2 细胞暴露于 QD（6 nm）和不同大小（15-20、50 和 100 nm）的 NPs 时，活性氧 (ROS) 的产生及其参与细胞凋亡。在 25–200 μg/mL 的浓度下，NPs 在 HepG2 细胞中诱导剂量依赖性细胞毒性。工程化的 NPs 以剂量和大小依赖性方式增加氧化应激，如 ROS 产生增加、脂质过氧化和谷胱甘肽减少所见。此外，用不同大小的 NPs 处理的 HepG2 细胞的细胞周期分析显示，在 24 小时暴露期后，凋亡峰增加。定量实时 PCR 数据显示 p53、bax 和 caspase-3 等凋亡标记基因的 mRNA 水平上调，而抗凋亡基因 bcl-2 的 mRNA 水平下调；因此，细胞凋亡是通过 p53、bax、caspase-3 和 bcl-2 途径介导的，这表明 ZnO 的 QD 和 NP 介导其毒性的可能机制。图形摘要