Chemical carcinogenicity of neodymium nitrate in AML12 hepatocytes: Dose-response metabolomics and sensitive biomarker identification.

This study aims to investigate the chemical carcinogenic toxicity of neodymium nitrate (Nd(NO3)3) in mouse hepatocytes AML12 using dose-response metabolomics. Specifically, our objectives are to: Identify key metabolites that respond to Nd(NO3)3 exposure. Elucidate the mechanisms underlying Nd(NO3)3-induced liver toxicity. Provide a scientific basis for risk assessment of Nd(NO3)3 exposure. AML12 cells were exposed to different concentrations of Nd(NO3)3 (0, 0.2, 0.4, and 0.8 µM) for 24 h. Metabolite changes were analyzed using UPLC-MS, and differential metabolites (DMs) were identified. Key metabolic pathways affected by Nd(NO3)3 include amino acid metabolism, nucleotide metabolism, and energy metabolism. Significant changes in these pathways suggest that Nd(NO3)3 induces metabolic disturbances that may lead to cytotoxicity. We identified potential biomarkers, such as UDP-N-acetylglucosamine, L-glutathione, and glycine, which exhibit dose-dependent responses. These findings provide insights into the mechanisms of Nd(NO3)3-induced chemical carcinogenicity and offer a scientific basis for risk assessment. Future research should further explore the toxicity and mechanisms in in vivo settings.

CONCLUSION

Our study reveals that Nd(NO3)3 induces metabolic disturbances in AML12 hepatocytes, leading to potential cytotoxicity. The identified potential biomarkers, such as UDP-N-acetylglucosamine, L-glutathione, and glycine, provide a basis for early detection and risk assessment of Nd(NO3)3 exposure. Further in vivo studies are needed to explore the long-term effects and mechanisms of Nd(NO3)3 toxicity.