Potent cytotoxicity and induction of ROS-mediated genomic instability, mitochondrial dysfunction, and apoptosis by Y2O3 NPs in Hep-G2 hepatic cancer cells

Abstract

Hepatic cancer, one of the most prevalent and lethal cancers globally, remains a significant health challenge, with limited treatment options underscoring the urgent need for novel, more effective therapies. Yttrium oxide nanoparticles (Y 2 O 3 NPs) have attracted attention in nanomedicine due to their promising properties, including enhanced drug delivery, imaging capabilities, and therapeutic effects. However, the specific impact of Y 2 O 3 NPs on hepatic cancer is largely unexplored. Therefore, this study was conducted to assess the cytotoxic effects of Y 2 O 3 NPs on cell viability, reactive oxygen species (ROS) generation, genomic stability, mitochondrial integrity, and apoptosis induction in Hep-G2 hepatic cancer cells. The results from the SRB cytotoxicity assay demonstrated a strong concentration-dependent decrease in Hep-G2 cell viability, with a notably low half-maximal inhibitory concentration (IC50) value of 13.15 µg/ml. Exposure to the IC50 concentration of Y 2 O 3 NPs led to increased ROS generation, DNA damage induction, and loss of mitochondrial membrane potential. Furthermore, the expression of pro-apoptotic p53 and mitochondrial ND3 genes was significantly upregulated, while the anti-apoptotic Bcl-2 gene was markedly downregulated, triggering apoptosis in Hep-G2 cells after 72 h of exposure to Y 2 O 3 NPs. Collectively, these findings highlight the therapeutic potential of Y 2 O 3 NPs in hepatic cancer, emphasizing the need for further research to fully explore their efficacy as a treatment option for liver cancer.

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