双酚是一种酚类化学品，常用于生产各种消费品。由于广泛接触，这些化合物可能对人类造成多种毒性作用。本研究旨在评估氧化锌纳米粒子 (ZnONPs) 对双酚 S (BPS) 诱导的人睾丸胚胎癌细胞系 (NT2/D1) 细胞毒性的保护作用。在本实验研究中，ZnONPs 和 BPS 的细胞毒性浓度对NT2/D1 细胞使用 MTT 测定进行优化。此后，ZnONPs（50和500μM）、BPS（300和600μM）以及用ZnONPs（50μM）预处理然后暴露于BPS（600μM）对SOX2和OCT4基因表达和细胞凋亡的影响分别使用定量逆转录酶聚合酶链式反应 (qRT-PCR) 和蛋白质印迹法评估相关蛋白（即 Bax 和 Bcl-2）。BPS 和 ZnONP 均在一定时间和剂量内降低 NT2/D1 细胞的活力依赖方式。用 50 μM ZnONP 预处理可增加 SOX2 和 OCT4 的 mRNA 水平，并改善因暴露于 BPS 半数抑制浓度 (IC50) 引起的细胞活力降低 (P<0.001)。此外，ZnONPs 预处理能够抑制 BPS 诱导的细胞凋亡，Bcl-2 蛋白水平增加（P<0.05）和 Bax 蛋白水平降低（P<0.001）证明了这一点。低浓度的 ZnONPs 可以通过调节 NT2/D1 细胞中凋亡相关蛋白和多能基因的表达来预防 BPS 的细胞毒性作用，建议进一步研究来证实这些结果。

Bisphenols are a type of phenolic chemical frequently used in producing various consumer products. Owing to their widespread exposure, these compounds can cause multiple toxic effects in humans. This study aimed to assess the protective effects of zinc oxide nanoparticles (ZnONPs) against bisphenol S (BPS)-induced cytotoxicity in the human testicular embryonic carcinoma cell line (NT2/D1).In this experimental study, cytotoxic concentrations of ZnONPs and BPS on NT2/D1 cells were optimized using the MTT assay. Thereafter, the effects of ZnONPs (50 and 500 μM), BPS (300 and 600 μM), and pre-treatment with ZnONPs (50 μM) followed by exposure to BPS (600 μM) on the expression of SOX2 and OCT4 genes and apoptosis-related proteins (i.e. Bax and Bcl-2) were evaluated, using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blotting, respectively.Both BPS and ZnONPs reduced the viability of NT2/D1 cells in a time- and dose-dependent manner. Pretreatment with 50 μM of ZnONPs increased mRNA levels of SOX2 and OCT4 and improved the reduction of cell viability caused by exposure to half-maximal inhibitory concentration (IC50) of BPS (P<0.001). In addition, pre-treatment with ZnONPs was able to suppress BPS-induced apoptosis, as evidenced by increased Bcl-2 (P<0.05) and decreased Bax (P<0.001) protein levels.Although our findings indicate that short-term treatment with a low concentration of ZnONPs could have beneficial effects in preventing the cytotoxic effects of BPS by modulating the expression of apoptosis-related proteins and pluripotent genes in the NT2/D1 cells, further studies are recommended to confirm these results.