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Superoxide-driven aconitase FE-S center cycling

P R Gardner1

  • 1Division of Critical Care, Children's Hospital Research Foundation, Cincinnati, Ohio 45229, USA.

Bioscience Reports
|February 1, 1997
PubMed
Summary

Superoxide (O2-) inactivates iron-sulfur enzymes like aconitase. This inactivation-reactivation cycle in cells monitors oxidative stress and impacts energy production. This process is crucial for cellular health.

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Nitric oxide sensitivity of the aconitases.

The Journal of biological chemistry·1997

Area of Science:

  • Biochemistry
  • Cell Biology
  • Enzymology

Background:

  • Cellular respiration generates superoxide (O2-), a reactive oxygen species.
  • Superoxide inactivates iron-sulfur cluster-containing enzymes, such as aconitase, a key citric acid cycle enzyme.
  • This inactivation involves iron release and [4Fe-4S] cluster oxidation, leading to loss of catalytic function.

Purpose of the Study:

  • To investigate the inactivation and reactivation mechanisms of aconitase by reactive oxygen species.
  • To establish aconitase activity as a sensitive indicator of cellular oxidative stress.
  • To explore the physiological and pathophysiological implications of aconitase cycling.

Main Methods:

  • Studied the effects of superoxide and other oxidants on aconitase activity in bacterial and mammalian systems.
  • Monitored iron release and [4Fe-4S] cluster status during inactivation.
  • Assessed the role of iron-sulfur cluster reduction and Fe2+ insertion in reactivation.

Main Results:

  • Aconitase is inactivated by superoxide and other oxidants (O2, H2O2, NO, ONOO-).
  • Inactivation involves the release of iron and oxidation of the [4Fe-4S] cluster.
  • Rapid reactivation occurs through cluster reduction and iron re-insertion, forming a dynamic cycle.
  • The balance of active/inactive aconitase reflects cellular O2- levels under stress.

Conclusions:

  • Aconitase inactivation-reactivation is a dynamic process modulating enzyme activity in response to oxidative stress.
  • Aconitase serves as a sensitive cellular biosensor for superoxide levels.
  • Oxidant-induced loss of aconitase activity can impair energy metabolism and exacerbate oxidative damage.
  • Iron-sulfur cluster cycling may have adaptive roles in gene expression and metabolic signaling.

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