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Hyperbaric oxygen rapidly produces intracellular bioenergetics dysfunction in human pulmonary cells. | LitMetric

Hyperbaric oxygen rapidly produces intracellular bioenergetics dysfunction in human pulmonary cells.

Chem Biol Interact

Department of Anesthesiology, The Ohio State University, Columbus, OH, 43210, USA; Center for Medical and Engineering Innovation, The Ohio State University, Columbus, OH, 43210, USA. Electronic address:

Published: December 2024

AI Article Synopsis

  • - This study investigates how short-term exposure to both high oxygen levels (hyperoxia) and increased pressure (hyperbaria) affects lung cells' mitochondria, which are vital for energy production.
  • - Researchers found that these exposures led to significant changes in mitochondrial movement, energy production, and protein levels linked to respiration, indicating signs of oxygen toxicity typically seen with longer exposures.
  • - The results highlight the potential health risks in environments with high oxygen and pressure, suggesting that this combined exposure can quickly disrupt cellular energy function, which could be useful for further research on oxygen toxicity and testing new treatments.

Article Abstract

Hyperoxic exposure lasting days alters mitochondrial bioenergetic and dynamic functions in pulmonary cells as indices of oxygen toxicity. The aim of this study was to examine effects of short duration hyperbaric and hyperoxic exposures to induce oxygen toxicity similarly. Cultured human lung microvascular endothelial cells, human pulmonary artery endothelial cells and A549 cells were exposed to hyperoxia (∼5 % CO equivalent, balance O) under hyperbaric conditions (4.8 ATA) for 1 and 4 h. Measures of mitochondrial dynamics, inner membrane potential, mitochondrial respiration, the intracellular distribution of bioenergetic capacity and respiration complex protein levels were then quantified. Exposures resulted in altered mitochondrial motility, presence of inhomogeneities in respiration parameters, loss of inner membrane potential, and changes in intracellular partitioning of ATP-linked respiration. Changes in the levels of respiration complex protein levels were also found. The combination of hyperoxic exposure with hyperbaric conditions rapidly produced changes in mitochondrial dynamics and bioenergetics in pulmonary cells. These changes are consistent with the onset of pulmonary oxygen toxicity previously known to result from long duration exposure to hyperoxia alone. These findings suggest health caution is warranted in environmental settings in which both hyperoxic and hyperbaric conditions are present. The synergism of hyperoxia and hyperbaria for rapid induction of oxygen toxicity in cellular models has utility for the study of mechanistic determinants of oxygen toxicity, testing of putative therapeutics, and associated investigations of mitochondrial dysfunction.

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Source
http://dx.doi.org/10.1016/j.cbi.2024.111266DOI Listing

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