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Related Experiment Videos

Disulfiram inhibits TNF-alpha-induced cell death.

A Zhao1, Z Q Wu, M Pollack

  • 1Departments of Medicine, Uniformed Services University, Bethesda, MD 20814, USA.

Cytokine
|September 8, 2000
PubMed
Summary

Disulfiram effectively inhibits tumor necrosis factor-alpha (TNF-alpha)-induced cell death by preserving mitochondrial function and reducing reactive oxygen species. This alcohol deterrent also blocks DNA fragmentation in vivo.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Disulfiram, an alcohol deterrent, is known to inhibit caspase-3 and DNA fragmentation.
  • Tumor necrosis factor-alpha (TNF-alpha) can induce significant cell death.
  • Investigating disulfiram's protective effects against TNF-alpha-induced cell death is crucial.

Purpose of the Study:

  • To determine if disulfiram inhibits TNF-alpha-induced cell death in vitro and in vivo.
  • To elucidate the mechanisms underlying disulfiram's protective effects.

Main Methods:

  • LLC-PK1 cells and murine liver models were used.
  • Cells were treated with TNF-alpha and varying doses of disulfiram.
  • Mitochondrial membrane potential and reactive oxygen species (ROS) were measured.

Related Experiment Videos

  • In vivo studies involved TNF-alpha and D-galactosamine treatment in mice.

    • Main Results:

    • Disulfiram demonstrated dose-dependent inhibition of TNF-alpha-induced cell death and caspase-3-like activity.
    • Disulfiram retained 80% efficacy even when added 4 hours after TNF-alpha.
    • Treatment with disulfiram restored mitochondrial membrane potential and suppressed ROS.
    • In vivo, disulfiram abolished TNF-alpha and D-galactosamine-induced hepatic DNA fragmentation and caspase-3-like activity.

    Conclusions:

    • Disulfiram is a potent inhibitor of TNF-alpha-induced cell death.
    • Mechanisms include stabilization of mitochondrial membrane potential, ROS suppression, and caspase-3 inhibition.
    • Disulfiram effectively inhibits DNA fragmentation in vivo via caspase-3 blockade.