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Oxygen toxicity causes cyclic damage by destabilizing specific Fe-S cluster-containing protein complexes.

Alan H Baik1, Augustinus G Haribowo2, Xuewen Chen3

  • 1Department of Medicine, Division of Cardiology, University of California, San Francisco, San Francisco, CA 94143, USA; Gladstone Institutes, San Francisco, CA 94158, USA.

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Excess oxygen (hyperoxia) damages key cellular proteins containing iron-sulfur clusters (ISC), impairing vital functions like energy production. This damage creates a cycle of toxicity, impacting lung health and other conditions.

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DNA damageFe-S clustershyperoxialung injurymitochondriaoxygenpurine synthesisredoxtranslation fidelity

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Physiology

Background:

  • Oxygen is essential for life but toxic at high concentrations (hyperoxia).
  • The molecular mechanisms underlying oxygen toxicity are not fully understood.
  • Iron-sulfur cluster (ISC) proteins are crucial for many cellular processes.

Purpose of the Study:

  • To systematically investigate cellular pathways affected by hyperoxia.
  • To identify the specific molecular targets of oxygen toxicity.
  • To elucidate the role of ISC proteins in hyperoxia-induced damage.

Main Methods:

  • Systematic investigation of cellular pathways.
  • Analysis of protein stability in hyperoxia.
  • Use of primary human lung cells and a mouse model (Ndufs4 KO).
  • Assessment of mitochondrial oxygen consumption and electron transport chain (ETC) function.

Main Results:

  • Hyperoxia destabilizes specific ISC-containing proteins.
  • Impaired functions include diphthamide synthesis, purine metabolism, nucleotide excision repair, and ETC function.
  • The ETC is highly vulnerable, leading to decreased mitochondrial oxygen consumption and a cycle of damage.
  • ETC dysfunction exacerbates hyperoxia sensitivity and ISC damage.

Conclusions:

  • Hyperoxia induces cellular damage by destabilizing ISC proteins, particularly affecting the ETC.
  • A feedback loop of mitochondrial dysfunction and tissue hyperoxia contributes to toxicity.
  • Findings have implications for understanding and treating hyperoxia-related pathologies.