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Ferric iron potentiates cell depolarization by a circulating shock protein
B J Eastridge1, J A Evans, D N Darlington
1Department of Surgery, University of Maryland School of Medicine, Baltimore.
Archives of Surgery (Chicago, Ill. : 1960)
|March 1, 1994
Summary
Iron, specifically ferric iron (Fe3+), enhances the activity of a shock protein found in plasma after hemorrhage. This protein may contribute to fluid shifts in shock by affecting intracellular salt and water balance.
Area of Science:
- Biochemistry
- Physiology
- Molecular Biology
Background:
- A circulating shock protein appears in plasma following hemorrhage.
- The function and regulation of this shock protein are not fully understood.
- Iron's role in modulating protein activity is a key area of investigation.
Purpose of the Study:
- To investigate the effect of iron on the depolarizing activity of a circulating shock protein.
- To determine if iron influences the protein's function in post-hemorrhage plasma.
Main Methods:
- Utilized a randomized laboratory design with male Sprague-Dawley rats.
- Induced hemorrhage and collected plasma for analysis.
- Purified the circulating shock protein and measured its depolarizing activity using an oxonol dye assay in the presence of different iron forms (Fe3+, Fe2+) and an iron chelator.
Main Results:
- Ferric iron (Fe3+), but not ferrous iron (Fe2+), potentiated the protein's depolarizing activity at physiological concentrations.
- An iron chelator abolished the protein's activity.
- Purification removed most activity, but Fe3+ restored it, indicating iron's crucial role.
Conclusions:
- Physiological concentrations of Fe3+ modulate the depolarizing activity of the circulating shock protein.
- This iron-modulated protein may play a role in the intracellular accumulation of salt and water during shock.