LAUSR

Titanium dioxide nanoparticles (nano‐TiO2) is one of the most widely used and produced nanomaterials. Studies have demonstrated that nano‐TiO2 could induce hepatotoxicity through oxidative stress, and lycopene has strong antioxidant capacity. The present study aimed to explore if lycopene protects the liver of mice from nano‐TiO2 damage. Ninety‐six ICR mice were randomly divided into eight groups. They were control group, nano‐TiO2‐treated group (50 mg/kg BW), lycopene‐treated groups (5, 20, and 40 mg/kg BW), and 50 mg/kg BW nano‐TiO2‐ and lycopene‐co‐treated groups (nano‐TiO2 + 5 mg/kg BW of lycopene, nano‐TiO2 + 20 mg/kg BW of lycopene, nano‐TiO2 + 40 mg/kg BW of lycopene). After treated by gavage for 30 days, the histopathology of the liver was observed. Liver function was evaluated using changes in serum biochemical indicators of the liver (AST, ALT, ALP); and the level of ROS was indirectly reflected by the level of SOD, GSH‐Px, MDA, GSH, and T‐AOC. TUNEL assay was performed to examine the apoptosis of hepatocytes. Proteins of p53, cleaved‐caspase 9, cleaved‐caspase 3, Bcl‐2, and Bax as well as p38 were detected. Results showed that lycopene alleviated the liver pathological damage and reduced the injury to liver function induced by nano‐TiO2, as well as decreased nano‐TiO2‐induced ROS. Meanwhile, lycopene mitigated apoptosis resulting from nano‐TiO2, accompanied by the reversed expression of apoptosis‐related proteins. Furthermore, lycopene significantly reversed the upregulation of p‐p38 induced by nano‐TiO2. In conclusion, this study demonstrated that nano‐TiO2 resulted in hepatocyte apoptosis through ROS/ROS‐p38 MAPK pathway and led to liver function injury. Lycopene protected mice liver against the hepatotoxicity of nano‐TiO2 through antioxidant property.