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Related Experiment Videos

Actin polymerization in cellular oxidant injury.

D B Hinshaw1, J M Burger, T F Beals

  • 1Department of Surgery, VA Medical Center, Ann Arbor, Michigan 48105.

Archives of Biochemistry and Biophysics
|August 1, 1991
PubMed
Summary

Oxidative stress triggers actin polymerization in cells, independent of microfilament breakdown. This actin assembly is linked to cellular sulfhydryl oxidation, not glutathione levels.

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Oxidative Stress Research

Background:

  • Cellular exposure to oxidants causes ATP-dependent microfilament disruption.
  • This disruption does not necessitate a net change in polymerized actin levels.
  • However, oxidant-injured cells sometimes show increased polymerized actin, prompting further investigation.

Purpose of the Study:

  • To investigate the conditions leading to actin polymerization in oxidant-exposed cells.
  • To determine the relationship between sulfhydryl oxidation and actin assembly.
  • To differentiate this polymerization from ATP-dependent microfilament disruption.

Main Methods:

  • Utilized P388D1 cell line exposed to hydrogen peroxide (H2O2) and diamide.
  • Measured oxidized glutathione (GSSG) formation as an indicator of sulfhydryl oxidation.

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  • Assessed actin polymerization using DNase I and flow cytometry assays.
  • Conducted experiments with glutathione (GSH)-depleted cells.

    • Main Results:

    • Significant actin polymerization occurred only under conditions of sulfhydryl oxidation post-oxidant exposure.
    • Early and greater sulfhydryl oxidation correlated with increased rate and extent of actin polymerization.
    • Actin polymerization was independent of glutathione depletion or absolute GSSG levels.

    Conclusions:

    • Oxidizing conditions inducing significant cellular sulfhydryl oxidation correlate with actin polymerization.
    • This actin assembly process is distinct from the ATP-dependent disruption of microfilaments.
    • Sulfhydryl oxidation, rather than glutathione status, appears to be the key factor driving this actin polymerization.