| Description |
Neodymium has been shown to induce genotoxicity in mice, but the molecular mechanisms behind this effect are not fully understood. To clarify the genotoxic effects of intragastric neodymium nitrate (Nd(NO3)3) administration over 28 consecutive days, we assessed the percentage of tail DNA in mouse hepatocytes using the alkaline comet assay, genetic toxicological biomarkers, and the expression levels of genes and proteins related to the p53 pathway in the mouse liver. Our results indicated significant accumulation of Nd(NO3)3 in the livers and kidneys of mice, resulting in micronuclei formation and DNA double-strand breaks, as indicated by comet and γ-H2AX assays, as well as DNA damage in hepatocytes. Nd(NO3)3 significantly increased the percentage of tail DNA in hepatocytes as measured by the alkaline comet assay and upregulated the expression of p53 pathway-related molecules, including ATM, Wip1, ATR, Chk2, MDM2, p53, p21, and NF-kB, at both the transcriptional and translational levels. This treatment effectively triggered the production of reactive oxygen species (ROS), 8-hydroxy-2'-deoxyguanosine (8-OHdG), and γ-H2AX in liver tissue. These findings suggest that Nd(NO3)3 induces hepatic genotoxicity and injury in mice, and modulates the expression of genes associated with DNA damage response, carcinogenesis, and inflammatory processes. |
