One Electron Reduction of Vanadate(V) to Oxovanadium(IV) by Low-Molecular-Weight Biocomponents Like Saccharides and Ascorbic Acid: Effect of Oxovanadium(IV) Complexes on pUC18 DNA and on Lipid Peroxidation in Isolated Rat Hepatocytes

1996 ◽  
Vol 224 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Alavattam Sreedhara ◽  
Nobuyuki Susa ◽  
Anjali Patwardhan ◽  
Chebrolu P. Rao
Keyword(s):  
Lipid Peroxidation ◽  
Molecular Weight ◽  
Ascorbic Acid ◽  
Rat Hepatocytes ◽  
Low Molecular Weight ◽  
Isolated Rat Hepatocytes ◽  
Acid Effect ◽  
Electron Reduction ◽  
Isolated Rat

Effects of Deoxycholic Acid and Its Epimers on Lipid Peroxidation in Isolated Rat Hepatocytes

2001 ◽  
Vol 129 (5) ◽  
pp. 683-689 ◽  
Author(s):  
A. Hino ◽  
M. Morita ◽  
M. Une ◽  
K. Fujimura ◽  
T. Kuramoto
Keyword(s):  
Lipid Peroxidation ◽  
Deoxycholic Acid ◽  
Rat Hepatocytes ◽  
Isolated Rat Hepatocytes ◽  
Isolated Rat

Molecular cytotoxic mechanisms of chlorpromazine in isolated rat hepatocytes

2013 ◽  
Vol 91 (1) ◽  
pp. 56-63 ◽  
Author(s):  
Stephanie L. MacAllister ◽  
Cheryl Young ◽  
Anna Guzdek ◽  
Nickholas Zhidkov ◽  
Peter J. O'Brien
Keyword(s):  
First Generation ◽  
Rat Hepatocytes ◽  
Antipsychotic Agents ◽  
Toxic Metabolite ◽  
Quinone Oxidoreductase ◽  
Metabolite Formation ◽  
Isolated Rat Hepatocytes ◽  
Electron Reduction ◽  
Catalyzed Oxidation ◽  
Isolated Rat

Chlorpromazine (CPZ), a member of the largest class of first-generation antipsychotic agents, is known to cause hepatotoxicity in the form of cholestasis and hepatocellular necrosis in some patients. The mechanism of CPZ hepatotoxicity is unclear, but is thought to result from reactive metabolite formation. The goal of this research was to assess potential cytotoxic mechanisms of CPZ using the accelerated cytotoxicity mechanism screening (ACMS) technique with freshly isolated rat hepatocytes. This study identified CPZ cytotoxicity and inhibition of mitochondrial membrane potential (MMP) to be concentration-dependent. Furthermore, inhibition of cytochrome P450s (CYPs), including CYP2D1 and 1A2, delayed CPZ cytotoxicity, suggesting a role for CYP activation of CPZ to a toxic metabolite(s) in this model. Metabolism studies also demonstrated glucuronide and glutathione (GSH) requirement for CPZ detoxification in hepatocytes. Inactivating the 2-electron reduction pathway, NAD(P)H quinone oxidoreductase (NQO1), caused a significant increase in hepatocyte susceptibility to CPZ, indicating quinoneimine contribution to CPZ cytotoxicity. Nontoxic concentrations of peroxidase/H2O2 (inflammatory model) increased cytotoxicity in CPZ-treated hepatocytes and caused additional mitochondrial toxicity. Inflammation further depleted GSH and increased oxidized glutathione (GSSG) levels. Results suggest activation of CPZ to reactive metabolites by 2 pathways in hepatocytes: (i) a CYP-catalyzed quinoneimine pathway, and (ii) a peroxidase-catalyzed oxidation of CPZ to CPZ radicals.

Lipid peroxidation in isolated rat hepatocytes measured by ethane and n-pentane formation

1982 ◽  
Vol 49 (3-4) ◽  
pp. 265-273 ◽  
Author(s):  
N. de Ruiter ◽  
H. Ottenwälder ◽  
H. Muliawan ◽  
H. Kappus
Keyword(s):  
Lipid Peroxidation ◽  
Rat Hepatocytes ◽  
Isolated Rat Hepatocytes ◽  
Isolated Rat

scholarly journals Copper Toxicity and Lipid Peroxidation in Isolated Rat Hepatocytes: Effect of Vitamin E

1989 ◽  
Vol 25 (1) ◽  
pp. 55-62 ◽  
Author(s):  
Ronald J Sokol ◽  
Michael W Devereaux ◽  
Maret G Traber ◽  
Robert H Shikes
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Copper Toxicity ◽  
Rat Hepatocytes ◽  
Isolated Rat Hepatocytes ◽  
Isolated Rat
Sign in / Sign up

Export Citation Format

Share Document