This study aimed to investigate the potential hepatotoxic effects of titanium dioxide nanoparticles (TiO2 NPs) on neonatal NMRI mice through maternal milk exposure. A total of 20 postpartum dams were divided into two groups: the experimental group received 30 mg/kg of TiO2 NPs, while the control group received deionized water for 14 days. The offspring were analyzed for oxidative stress markers, bioaccumulation, and histopathological changes in hepatic tissues. The results showed no significant difference in body weight or liver-to-body weight ratio between the treatment and control groups. However, oxidative stress was evident in the treatment group, with a significant reduction in glutathione (GSH) levels (0.8 µmol/g tissue, p<0.05) and glutathione peroxidase (GPx) activity (3.68 u/g tissue, p<0.05), compared to the control group. Additionally, malondialdehyde (MDA) levels, indicative of lipid peroxidation, were significantly higher in the treatment group (96 nmol/g tissue, p<0.001). TiO2 content was markedly increased in the treatment group’s liver (22.4 ng/g tissue, p<0.001) and stomach milk (41.6 ng/g tissue, p<0.001), suggesting bioaccumulation. Histological analysis revealed pronounced tissue degeneration and vascular changes in the treatment group’s hepatic tissues, contrasting with the normal histology observed in the control group. These findings indicate that maternal ingestion of TiO2 NPs can lead to oxidative stress and potential hepatotoxicity in neonatal mice, with significant implications for environmental and consumer product safety regulations.

The extensive application of silver nanoparticles (AgNPs) has been increased due to their antimicrobial properties, however numerous concerns has been arisen about their toxicity potential. Since nanoparticles can cross through the placenta and accumulate in the embryonic organs especially liver, in this study, developmental hepatotoxicity of AgNPs was investigated.Pregnant rats were divided into two groups, vehicle control group and treated group. Treated group received AgNPs (25 mg/Kg) through intra-gastric gavage in a period of gestational days1-19. Pups were sacrificed after the birth and their livers collected. Histopathology, ICP- mass spectrometry, Spectrophotometric assay, and ELISA were employed to evaluate AgNPs toxicity in the liver of pups.Glutathione peroxidase (GPX) activity and glutathione (GSH) level were significantly decreased and malondialdehyde (MDA) and caspase 9 levels were significantly increased, although there was no significant change in caspase 8 content in the liver of offspring. Fattydegeneration and congested dilated sinusoids were also observed in histo-pathological examination.These results suggest that maternal oral exposure to AgNPs may induce oxidative stress and apoptosis in the liver of their offspring. Further investigations are required to clarify molecular events behind this happening.