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Role of iron metabolism in hemorrhagic shock - interplay of heme oxygenases and nitric oxide synthases

Abstract
Multi organ failure is still the major cause of late death in patients with severe blood loss after trauma or injury. The underlying mechanism leading to this sometimes fatal complication are multifactorial but in detail not fully understood. It is possible that iron ions (LMW iron) participate in the generation of so called oxidative stress during resusciation which can lead to cell damage and subsequent organ dysfunction. On the other hand LMW iron participates in gene regulation and immune cell function. However, it is not clear to what extent LMW iron contributes to organ damage that occurs in patients of shock due to excessive blood loss. To clarify this is one aim of this study. Additionally we want to find out to what extent modulation of the iron metabolism would improve the clinical outcome of patients in this pathologic situation. Therefore we want to modulate two important enzyme systems NOS (nitric oxide synthases) and heme oxygenases (HO). These enzyme systems are linked to each other and have distinct roles affecting the availability and toxicity of LMW iron. Both enzyme systems are diversely implicated in mechanisms leading to cell and organ damage. We expect that modulating the NOS/HO system during early treatment of trauma patients with severe blood loss will decrease the extent of organ damage. On the base of these investigations it will be possible to adjust medicamentation such that more of these severely affected patients will survive.
Project leader
Duvigneau Catharina
Duration
01.09.06-31.08.08
Type of Research
Basic research
Vetmed Research Units
Institute for Medical Biochemistry
Projekt partner
Ludwig Boltzmann Institut für experimentelle und klinische Traumatologie, Donaueschingenstraße 13, A-1200 Wien, Austria
Universität des Saarlandes, Kirrberger Straße, D Homburg, Saarbrücken, Germany
Funded by
European Shock Society, , European Union
4 Publications

Duvigneau, JC; Hartl, RT; Gemeiner, M; Moldzio, R; Bahrami, S; Kozlov, AV (2006): Hemoxygenase products inhibit polymerase reactions. 12th Congress of the European Shock Society, Ulm, GERMANY, Germany, SEP 14-16, 2006. Shock (26) 25-25.

Kozlov, A.V; Duvigneau, J.C; Piskernik, C; Hartl, R.T; Haindl, S; Kehrer, I; Ebel, T; Gemeiner, M; Redl, H (2006): Loss of mitochondrial function under Endotoxic shock is likely due to hemohygenase mediated increase in free iron levels. Life Sciences 2006, Salzburg, Austria, 25.-27.09. 2006. Life Sciences 2006, Salzburg, 25.-27.09. 2006.

Duvigneau, J.C; Piskernik, C; Hartl, R.T; Haindl, S; Kehrer, I; Ebel, T; Gemeiner, M; Redl, H; Kozlov, A.V (2006): Increase of catalytically active "free" iron in the liver of rats subjected to endotoxic shock. XIII Biennial Meeting of the Society for Free Radical Research International, Davos, Schweiz, Switzerland, 15.-19. August 2006. XIII Biennial Meeting of the Society for Free Radical Research International, Davos, Schweiz, 15.-19. August 2006.

Duvigneau, J.C; Piskernik, C; Hartl, R.T; Haindl, S; Kehrer, I; Ebel, T; Gemeiner, M; Redl, H; Kozlov, A (2006): Endotoxin mediated expression of hemoxygenase in rats is likely a source of free iron, impairing mitochondrial function. Shock 26,(Suppl. 1).

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