Article Text

  1. D Brait1,
  2. M Sifringer1,
  3. B Gerstner1,
  4. F Brehmer1,
  5. M Dzietko1,
  6. A Kaindl2,
  7. U Felderhoff-Mueser1
  1. 1Department of Neonatology, Charite Universitaetsmedizin Berlin, Berlin, Germany
  2. 2Department of Neuropediatrics, Charite Universitaetsmedizin Berlin, Berlin, Germany


Background and Aims Oxygen toxicity contributes to the pathogenesis of cerebral palsy in survivors of preterm birth. We demonstrated previously that hyperoxia-induced apoptosis during infancy is associated with oxidative stress, decreased expression of neurotrophins and increase of pro-inflammatory cytokines. To explore further pathogenetic mechanisms of hyperoxia we investigated the impact of supraphysiologic oxygen levels on Latexin, a maker representing cortical connectivity and Glyoxalase 1, which is part of an antioxidant defence mechanism.

Methods Six day old rat pups were sacrificed after a 24 hour exposure with their mothers to 80% oxygen. Brains were either examined histologically to visualize degenerating cells (De Olmos silver and Fluoro Jade staining) or were processed for Western blotting and realtime PCR analysis.

Results Oxygen exposure triggered cell death. Western blotting and realtime PCR experiments demonstrated significant upregulation of Glyoxalase 1 and Latexin following oxygen exposure.

Conclusion These findings suggest that hyperoxia induces a change in the regulation of proteins involved in neuronal connectivity and oxidative stress in cortical structures.

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