Author/Authors :
Jing-Ying Xu، نويسنده , , Yuan-Yuan Su، نويسنده , , Jin-Sheng Cheng، نويسنده , , Shuxia Li، نويسنده , , Ruili Liu، نويسنده , , Wenxin Li، نويسنده , , Guo-Tong Xu، نويسنده , , Qingnuan Li، نويسنده ,
Abstract :
An important biologically-relevant property of fullerenol is its ability to quench free radicals. Carbon tetrachloride (CCl4)-induced hepatotoxicity and nephrotoxicity model was used to investigate the possible mechanisms of fullerenol protection in Sprague–Dawley rats in this study. Rats were administrated with fullerenol (0, 1, 1.5 and 5 mg/kg d) by intravenous or intraperitoneal injection for 3 days before CCl4 challenge, 24 h following the CCl4 challenge, all the rats were assessed using serum and tissue homogenates biomarkers as well as the pathological evaluation. All results showed that CCl4 caused significant increasing serum activity of alanine aminotransferase and aspartate aminotransferase, as well as the concentration of blood urea nitrogen and creatinine. Malondialdehyde level was also increased significantly, whereas the ratio of reduced glutathione to oxidized glutathione was decreased in tissue homogenates. The pathological evaluation indicated the liver and kidney were damaged by CCl4. Fullerenol-pretreatment alleviated biomarker changes as well as histological changes significantly, and fullerenol-pretreatment alone can increase the ratio of reduced glutathione to oxidized glutathione, which indicated fullerenol could protect tissues against CCl4-induced oxidative stress by improving the antioxidant ability.