[Oxidative damage and apoptosis in NIT-1 cells induced by ethanol]

Wei Sheng Yan Jiu. 2005 May;34(3):306-8.
[Article in Chinese]

Abstract

Objective: To decide whether ethanol induce apoptosis in mouse insulinoma cells (NIT-1) and the potential mechanism involved.

Methods: After NIT-1 cells were exposed to various concentrations of ethanol, agarose gel electrophoresis was used to detected DNA fragmentation. malondialdehyde (MDA) content, glutathione (GSH) level, superoxide dismutase(SOD) and glutathione peroxidase (GSH-Px) were measured in NIT-1 cells to evaluate the oxidative damage degree. Caspase-3 relative activity was determined by colorimetric assay.

Results: The results showed a "DNA ladder" pattern after treated with ethanol in NIT-1 cells. The MDA content was higher, the SOD activity, GSH-Px activity and GSH content were lower in ethanol group than those of control group. Ethanol increased the caspase-3 activity by a dose and time dependent manner.

Conclusion: Higher concentration of ethanol induces imbalance of oxidation and antioxidative ability in NIT-1 cells, and oxidative stress further leads to apoptosis which may be related to the increased caspase-3 activity.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Caspase 3 / metabolism
  • Cell Line, Tumor
  • Ethanol / toxicity*
  • Glutathione / metabolism
  • Glutathione Peroxidase / metabolism
  • Insulinoma / metabolism*
  • Insulinoma / pathology*
  • Malondialdehyde / metabolism
  • Mice
  • Mice, Transgenic
  • Oxidative Stress / drug effects*
  • Random Allocation
  • Superoxide Dismutase / metabolism

Substances

  • Ethanol
  • Malondialdehyde
  • Glutathione Peroxidase
  • Superoxide Dismutase
  • Casp3 protein, mouse
  • Caspase 3
  • Glutathione