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Alteration of Adenosine Triphosphate and Other Nudeotides After Sublethal Oxidant Injury to Rat Type II Alveolar Epithelial Cells

The alveolar epithelial cells of the lower respiratory tract are continuously exposed to injurious agents, including oxygen radicals. The type II alveolar epithelial cell is critically important to the normal function of the lung, because it is responsible for synthesis of surfactant and other essen...

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Bibliographic Details
Published in:The American journal of the medical sciences 1995-03, Vol.309 (3), p.140-145
Main Authors: Abernathy, Frank, Pacht, Eric R.
Format: Article
Language:English
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Summary:The alveolar epithelial cells of the lower respiratory tract are continuously exposed to injurious agents, including oxygen radicals. The type II alveolar epithelial cell is critically important to the normal function of the lung, because it is responsible for synthesis of surfactant and other essential duties. The present investigation measured the level of intracellular nucleotides and adenosine over time after exposure of type II cells to sublethal concentrations of physiologically relevant oxidants, hydrogen peroxide and hypochlorous acid (HOCl). Initially, it was determined that 250 μM HOCl or 250 μM hydrogen peroxide could each cause sublethal injury to the type II cells after exposure of up to 1 and 2 hours, respectively. After exposure to 250 μM hydrogen peroxide, the intracellular levels of adenosine, adenosine diphosphate, and adenosine triphosphate all initially increased in the first 1 to 15 minutes, but subsequently decreased significantly, ultimately reaching close to 40% below control levels. The level of adenosine monophosphate remained significantly elevated throughout the exposure until returning to control levels after 2 hours. Similar results occurred after the type II cells were exposed to 250 μM HOCl. This study demonstrates that adenosine triphosphate and other cellular nucleotides and nucleosides were decreased in type II cells before lethal injury and subsequent cell death.
ISSN:0002-9629
1538-2990
DOI:10.1097/00000441-199503000-00004