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Zinc inhibits ethanol-induced HepG2 cell apoptosis

Authors
Journal
Toxicology and Applied Pharmacology
0041-008X
Publisher
Elsevier
Publication Date
Volume
229
Issue
1
Identifiers
DOI: 10.1016/j.taap.2007.11.019
Keywords
  • Zinc
  • Ethanol
  • Apoptosis
  • Hepg2 Cells
  • Ros
  • Fas (Cd95)
  • Fasl
  • Caspases

Abstract

Abstract Alcohol consumption produces a variety of metabolic alterations in liver cells, associated with ethanol oxidation and with nonoxidative metabolism of ethanol, among others apoptosis of hepatocytes. As zinc is known as a potent antioxidant and an inhibitor of cell apoptosis, the aim of this paper was to investigate whether zinc supplementation could inhibit ethanol-induced HepG2 apoptosis, and whether this inhibition was connected with attenuation of oxidative stress and modulation of FasR/FasL system expression. The results indicated that zinc supplementation significantly inhibited ethanol-induced HepG2 cell apoptosis (measured by cytochrome c release from mitochondria and caspase-3 activation) by attenuation of reactive oxygen species (ROS) production, increase in the cellular level of GSH, inhibition of ethanol-induced sFasR and FasL overexpression and caspase-8 activation. These results indicate that zinc can inhibit ethanol-induced hepatocyte apoptosis by several independent mechanisms, among others by an indirect antioxidative effect and probably by inhibition of caspase-8 and caspase-9 activation.

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