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A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells
Published on: April 11, 2014
Ascorbic acid abrogates microparticle generation and vascular injuries associated with high-pressure exposure
Ming Yang1, Veena M Bhopale1, Stephen R Thom2
1Department of Emergency Medicine, University of Maryland, Baltimore, Maryland.
Abstract:
We hypothesized that pathological changes associated with elevations in annexin V-positive microparticles (MPs) following high-pressure exposures can be abrogated by ascorbic acid in a murine model. Mice exposed for 2 h to 790-kPa air and killed at 2 or 13 h postdecompression exhibited over threefold elevations in circulating MPs, as well as subgroups bearing Ly6G, CD41, Ter119, CD31, and CD142 surface proteins. There was evidence of significant neutrophil activation, platelet-neutrophil interactions, and vascular injury to brain, omentum, psoas, and skeletal muscles assessed as leakage of high-molecular-weight dextran. Prophylactic ascorbic acid (500 mg/kg ip) administration prevented all postdecompression neutrophil changes and vascular injuries. Ascorbic acid administration immediately after decompression abrogated most changes, but evidence of vascular leakage in the brain and skeletal muscle at 13 h postdecompression persisted. No significant elevations in these parameters occurred after injection of ascorbic acid alone. The findings support the idea that MP production occurring with exposures to elevated gas pressure is an oxidative stress response and that antioxidants may offer protection from pathological effects associated with decompression.
Insights
High-pressure exposures increase microparticles (MPs) and cause vascular injury. Ascorbic acid (vitamin C) prevents these effects, suggesting MPs are an oxidative stress response.
Area of Science:
- Biomedical Science
- Physiology
- Toxicology
Background:
- High-pressure exposures can lead to pathological changes.
- Elevated circulating microparticles (MPs) are associated with these changes.
- Oxidative stress is implicated in decompression-related pathologies.
Purpose of the Study:
- To investigate the protective effects of ascorbic acid against pathological changes induced by high-pressure exposure.
- To determine if microparticle production is an oxidative stress response.
- To assess the efficacy of ascorbic acid administered before and after decompression.
Main Methods:
- Murine model exposed to 790-kPa air for 2 hours.
- Assessment of circulating MPs with specific surface protein markers (Ly6G, CD41, Ter119, CD31, CD142).
- Evaluation of neutrophil activation, platelet-neutrophil interactions, and vascular injury via dextran leakage.
Main Results:
- Decompression caused threefold elevations in circulating MPs and significant vascular injury in multiple organs.
- Prophylactic ascorbic acid (500 mg/kg) prevented all neutrophil changes and vascular injuries.
- Post-decompression ascorbic acid mitigated most, but not all, vascular leakage.
Conclusions:
- Microparticle production following high-pressure exposure is likely an oxidative stress response.
- Ascorbic acid demonstrates protective effects against decompression-induced pathology.
- Antioxidants may serve as a therapeutic strategy for decompression-related injuries.
