Learn More
Numerous studies have demonstrated that the brain is one of the target organs in acute or chronic titanium dioxide (TiO2) nanoparticles (NPs) toxicity, and oxidative stress plays an important role in this process. However, whether brain oxidative injury responds to TiO2 NPs by activating the P38-nuclear factor-E2-related factor-2 (Nrf-2) pathway is not(More)
Previous studies demonstrate that the exposure to titanium dioxide nanoparticles (TiO(2) NPs) damages the central nervous system of mice; however, very little is known about the effects of TiO(2) NPs on hippocampal apoptosis or its molecular mechanism. The present study investigated the molecular mechanism associated with hippocampal apoptosis in mice(More)
Titanium dioxide nanoparticles (TiO(2) NPs) are now in daily use including popular sunscreens, toothpastes, and cosmetics. However, the effects of TiO(2) NPs on human body, especially on the central nervous system, are still unclear. The aim of this study was to determine whether TiO(2) NPs exposure results in persistent alternations in nervous system(More)
Experimental studies have demonstrated that lanthanides could impair cognitive functions of children and animals, but very little is known about the hippocampal apoptosis and its molecular mechanism. The study investigated the signal pathway of hippocampal apoptosis induced by intragastric administration of CeCl(3) for 60 consecutive days. It showed that(More)
Cerium has been demonstrated to damage liver of mice, but very little is known about the molecular mechanisms underlying the mouse liver apoptosis. In order to understand the liver injury induced by intragastric administration of cerium chloride (CeCl3) for 60 consecutive days, the hepatocyte ultrasrtucture, various oxidative stress parameters, and the(More)
The organ toxicity of lanthanides (Ln) on organisms had been recognized, but very little is known about the oxidative injury of brain caused by Ln. In order to study the mechanisms underlying the effects of Ln on the brain, ICR mice were injected with a single 20 mg/kg body weight dose of LaCl(3), CeCl(3), and NdCl(3) into the abdominal cavity daily for 14(More)
To investigate the molecular mechanism of inflammatory response in the mouse liver caused by exposure to CeCl₃, we measured the liver indices, and cerium content, evaluated the liver histopathological section, detected serum biochemical parameters of liver function, and the immunoglobulin M (IgM) content, analyzed the liver mRNA and protein expression(More)
Numerous studies have demonstrated lanthanide (Ln) accumulation in the liver, and the corresponding damage; however, very little work has been done to evaluate the relationship between Ln-induced liver injury and its gene expression profile in mice. In this study, liver injury and gene-expressed profiles in male mice induced by oral administration of CeCl3(More)
While the hepatocyte apoptosis induced by TiO(2) nanoparticles (NPs) has been demonstrated, very little is known about the molecular mechanisms underlying this mouse liver apoptosis. In order to understand the hepatocyte apoptosis induced by intragastric administration of TiO(2) NPs for consecutive 60 days, the hepatocyte apoptosis, various oxidative stress(More)
In an effort to examine signaling pathway of inflammation of the mouse liver caused by intragastric administration of titanium dioxide nanoparticles (NPs), we assessed Toll-like receptor-2 (TLR2), TLR-4, IκB kinase (IKK-α, IKK-β), IκB nucleic factor-κB (NF-κB), NF-κBP52, NF-κBP65, tumor necrosis factor-α (TNF-α), NF-κB-inducible kinase (NIK), interleukin-2(More)