Journal
TOXICOLOGY AND APPLIED PHARMACOLOGY
Volume 185, Issue 3, Pages 172-179Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/taap.2002.9538
Keywords
fenofibrate; peroxisome proliferator-activated receptor (PPAR); HepG2; oxidative stress; intracellular calcium; mitochondrial membrane potential (MMP)
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The aim of this work was to investigate the effects of hypolipidemic agent fenofibrate (FF), a peroxisome proliferator (PP), on human HepG2 cells and to characterize the intracellular events involved. The results showed that, in contrast to the tumor-promoting effects in rodents, high FF concentrations induced human HepG2 cell death through a mechanism involving an increase in the levels of reactive oxygen species (ROS) and intracellular GSH depletion, which led, through mitochondrial dysfunction and perturbation of intracellular Ca2+ homeostasis, to cell death. The nuclear receptor peroxisome proliferator-activated receptor-alpha (PPARalpha) was expressed following FF treatment. The results suggest that, although long-term administration of PPs causes liver cancer in susceptible species (e.g., rodents), FF inhibits the growth of human HepG2 cells in a dose-related manner and oxidative stress was involved in this effect. (C) 2002 Elsevier Science (USA).
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