A toxicogenomics approach for risk assessment of glutathione depletion and oxidative stress-induced nongenotoxic hepatocarcinogenesis in the rat liver

2006 ◽  
Vol 164 ◽  
pp. S5-S6
Author(s):  
Takeki Uehara ◽  
Naoki Kiyosawa ◽  
Atsushi Ono ◽  
Toshikazu Miyagishima ◽  
Tetsuro Urushidani ◽  
...  
2004 ◽  
Vol 37 (11) ◽  
pp. 1718-1729 ◽  
Author(s):  
Bin Ji ◽  
Kousei Ito ◽  
Shuichi Sekine ◽  
Ai Tajima ◽  
Toshiharu Horie

2014 ◽  
Vol 39 (3) ◽  
pp. 344-350 ◽  
Author(s):  
Aysun Kilic Suloglu, PhD ◽  
Assoc. Prof. Gozde Girgin, PhD ◽  
Prof. Guldeniz Selmanoglu, PhD ◽  
Serdar Balci, MD ◽  
Prof. Terken Baydar, PhD

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Claudia Isabel García-Berumen ◽  
Omar Ortiz-Avila ◽  
Manuel Alejandro Vargas-Vargas ◽  
Bricia A. del Rosario-Tamayo ◽  
Clotilde Guajardo-López ◽  
...  

2013 ◽  
Vol 33 (5) ◽  
pp. 534-541 ◽  
Author(s):  
Y Li ◽  
Y Deng ◽  
Y Tang ◽  
H Yu ◽  
C Gao ◽  
...  

Accumulating evidence has shown that ethanol-induced iron overload plays a crucial role in the development and progression of alcoholic liver disease. We designed the present study to investigate the potential protective effect of quercetin, a naturally occurring iron-chelating antioxidant on alcoholic iron overload and oxidative stress. Ethanol-incubated (100 mmol/L) rat primary hepatocytes were co-treated by quercetin (100 µmol/L) and different dose of ferric nitrilotriacetate (Fe-NTA) for 24 h. When the hepatic enzyme releases in the culture medium, redox status of hepatocytes and the intercellular labile iron pool (LIP) level were assayed. Our data showed that Fe-NTA dose dependently induced cellular leakage of aspartate transaminase and lactate dehydrogenase, glutathione depletion, superoxide dismutase inactivation, and overproduction of malondialdehyde) and reactive oxygen species (ROS) of intact and especially ethanol-incubated hepatocytes. The oxidative damage resulted from ethanol, Fe-NTA, and especially their combined treatment was substantially alleviated by quercetin, accompanying the corresponding normalization of intercellular LIP level. Iron in excess, thus, may aggravate ethanol hepatotoxicity through Fenton-active LIP, and quercetin attenuated ethanol-induced iron and oxidative stress. To maintain intercellular LIP contributes to the hepatoprotective effect of quercetin besides its direct ROS-quenching activity.


2009 ◽  
Vol 65 (1) ◽  
pp. 41-54 ◽  
Author(s):  
Adrienne N. Howard ◽  
Kathleen A. Bridges ◽  
Raymond E. Meyn ◽  
Joya Chandra

Diabetes ◽  
1995 ◽  
Vol 44 (8) ◽  
pp. 992-998 ◽  
Author(s):  
R. A. Trocino ◽  
S. Akazawa ◽  
M. Ishibashi ◽  
K. Matsumoto ◽  
H. Matsuo ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document