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This study demonstrated that both copper oxide nanoparticles (CuO‐NPs) and copper nanoparticles (Cu‐NPs) can cause swelling, inflammation, and cause damage to the mitochondria of alveolar type II epithelial cells in mice. Cellular examinations indicated that both CuO‐NPs and Cu‐NPs can reduce cell viability and harm the mitochondria of human bronchial epithelial cells, particularly Beas‐2B cells. However, it is clear that CuO‐NPs exhibit a more pronounced detrimental effect compared with Cu‐NPs. Using bafilomycin A1 (Bafi A1), an inhibitor of lysosomal acidification, was found to enhance cell viability and alleviate mitochondrial damage caused by CuO‐NPs. Additionally, Bafi A1 also reduces the accumulation of dihydrolipoamide S‐acetyltransferase (DLAT), a marker for mitochondrial protein toxicity, induced by CuO‐NPs. This observation suggests that the toxicity of CuO‐NPs depends on the distribution of copper particles within cells, a process facilitated by the acidic environment of lysosomes. The release of copper ions is thought to be triggered by the acidic conditions within lysosomes, which aligns with the lysosomal Trojan horse mechanism. However, this association does not seem to be evident with Cu‐NPs. In mice, CuO‐NPs caused more extensive lung tissue damage than Cu‐NPs. In Beas‐2B cells, inhibition of lysosomal acidification with Bafi A1 markedly decreased CuO‐NPs‐induced mitochondrial damage. The lysosomal Trojan horse mechanism of aggravates CuO‐NPs‐induced cuproptosis in Beas‐2B cells, which can be reversed by Bafi A1. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of over-expression of nudix hydrolase 21 (NUDT21) on the proliferation of colon cancer HCT-116 cells and its mechanism. Methods The NUDT21 over-expression plasmid was constructed by Gibson assembly. The colony formation assay and CCK-8 assay were used to detect cell proliferation. The cell cycle of HCT-116 cells was detected by flow cytometry. Western blot was performed to detect the expressions of P53, cyclin-dependent kinase 2 (CDK2), phosphorylated retinoblastoma protein at serine 780 (p-Rb-Ser780), and p-Rb-Ser608. Results The sequencing results showed that the NUDT21 over-expression plasmid was successfully constructed. After the NUDT21 over-expression plasmid was transfected into HCT-116 cells, the expressions of NUDT21 mRNA and protein in the cells were significantly increased. The over-expression of NUDT21 inhibited the proliferation of HCT-116 cells and arrested the cell cycle in G0/G1 phase. The expressions of CDK2, p-Rb-Ser608, and p-Rb-Ser780 proteins decreased while the expression of P53 protein increased. Conclusion Over-expression of NUDT21 inhibits the proliferation of HCT-116 cells by blocking P53/CDK2/Rb signal pathway.