Influence of oxidation and crosslinking on oxygen binding properties of mouse erythrocytes

Lotero, L. Alfredo; Jordán, J.A.; López, Rosa; García-Pérez, Ana Isabel; Diez, José C.

doi:10.1002/cbf.901

Cited by 3 publications

(3 citation statements)

References 30 publications

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“…However, studies reporting this effect looked at much higher concentrations of diamide (2-5 mM) than those used in the present study (23). At a concentration of 100 M, diamide was shown to have no affect on hemoglobin O 2 saturation (37).…”

Section: Discussioncontrasting

confidence: 52%

The Rho kinase inhibitor Y-27632 increases erythrocyte deformability and low oxygen tension-induced ATP release

Thuet

Bowles

Ellsworth

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Low oxygen (O(2)) tension and mechanical deformation are stimuli for ATP release from erythrocytes. It has been shown previously that rabbit erythrocytes made less deformable with diamide, a thiol cross-linking agent, release less ATP in response to low O(2) tension, suggesting a link between these two stimuli. In nonerythroid cells, activation of the Rho/Rho kinase signaling pathway has been reported to decrease cell deformability by altering Rho kinase-dependent cytoskeleton-protein interactions. We investigated the hypothesis that the Rho kinase inhibitor Y-27632 would increase erythrocyte deformability and thereby increase low O(2) tension-induced ATP release from erythrocytes. Here we show that Y-27632 (1 μM) increases erythrocyte deformability (5%) and increases low O(2) tension-induced ATP release (203%) from healthy human erythrocytes. In addition, we found that, when erythrocytes were made less deformable by incubation with diamide (100 μM), Y-27632 restored both deformability and low O(2) tension-induced ATP release to levels similar to those measured in the absence of diamide. These findings suggest that the Rho kinase inhibitor Y-27632 is able to reverse the diamide-induced decrease in erythrocyte deformability and rescue low O(2) tension-induced ATP release. These results further support a link between erythrocyte deformability and ATP release in response to low O(2) tension.

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Section: Discussioncontrasting

confidence: 52%

The Rho kinase inhibitor Y-27632 increases erythrocyte deformability and low oxygen tension-induced ATP release

Thuet

Bowles

Ellsworth

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…7 Another potential concern with diamide is that treatment of mouse erythrocytes with diamide at concentrations of 2 mmol/L or greater was reported to induce a loss of cooperativity in the binding of O 2 by hemoglobin. 32 In another study using human erythrocytes, it was shown that there was a decrease in P 50 (O 2 tension at which hemoglobin is 50% saturated) when erythrocytes were treated with 5 mmol/L diamide, but no change in P 50 was observed when erythrocytes were treated with 2 mmol/L diamide. 15 To ensure that the far smaller concentration of diamide used in these studies (100 mmol/L) did not alter the ability of hemoglobin to bind or release O 2 , hemoglobin, O 2 saturations in the presence and absence of diamide were determined.…”

Section: Discussionmentioning

confidence: 98%

“…Another potential concern with diamide is that treatment of mouse erythrocytes with diamide at concentrations of 2 mM or greater was reported to induce a loss of cooperativity in the binding of O 2 by hemoglobin (37). In another study using human erythrocytes it was shown that a decrease in the P 50 (O 2 tension at which hemoglobin is 50% saturated) when erythrocytes were treated with 5 mM diamide but no change in P 50 was observed when erythrocytes were treated with 2 mM diamide (29).…”

Section: Discussionmentioning

confidence: 99%

Diamide decreases deformability of rabbit erythrocytes and attenuates low oxygen tension-induced ATP release

Sridharan

Sprague

Adderley

et al. 2010

Exp Biol Med (Maywood)

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Exposure of erythrocytes to reduced oxygen (O2) tension activates the heterotrimeric G protein Gi, resulting in accumulation of cAMP and release of ATP. The mechanism by which exposure of erythrocytes to reduced O2 tension activates Gi is not known. Here we investigate the hypothesis that, in rabbit erythrocytes, ATP release in response to exposure to reduced O2 tension requires membrane deformation. If this hypothesis is correct, then decreasing the deformability of the erythrocyte membrane should decrease the release of ATP in response to reduced O2 tension. We report that treating erythrocytes with diamide, a compound that decreases erythrocyte deformability, inhibits low O2 tension induced ATP release. Treating erythrocytes with diamide does not, however, interfere with cAMP accumulation or ATP release in response to a direct activator of Gi (mastoparan 7) or in response to receptor mediated activation of Gs (the prostacyclin analog, iloprost). These results demonstrate that diamide (100 μM) does not directly inhibit the signaling pathways for ATP release from rabbit erythrocytes and support the hypothesis that deformability of the erythrocyte membrane is required for low O2 tension-induced ATP release from these cells.

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Differential In vitro and In vivo Behavior of Mouse Ascorbate/Fe3+ and Diamide Oxidized Erythrocytes

et al. 2001

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Chemical oxidation of mouse erythrocytes has been carried out using two different oxidizing systems namely: Diamide and Ascorbate/Fe3+ together with different concentrations of the oxidant. These oxidation treatments produced different extents of modification in membrane proteins as was observed by electrophoretic analyses that showed a possible formation of high molecular weight aggregates. Lipid peroxidation was also observed as the result of these chemical treatments. The action of these two oxidation treatments produced different extents of lipid peroxidation in which the effect Ascorbate/Fe3+ reached higher values than that shown by diamide treatments. To study the resulting in vitro behavior of such oxidized erythrocytes, we have evaluated the recognition of oxidized erythrocytes by peritoneal macrophages. In the conditions used, diamide oxidized erythrocytes were more highly recognized by macrophages than Ascorbate/Fe3+ treated erythrocytes. However, in both cases an influence of serum factors in the recognition process can be inferred. Additionally, we have correlated on one side the action of different oxidation systems on mouse erythrocytes with different in vivo behavior and organ uptake of the oxidized erythrocytes. On the other side, differential targeting of oxidized erythrocytes to a liver or spleen was observed on dependence of the oxidant used.

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Influence of oxidation and crosslinking on oxygen binding properties of mouse erythrocytes

Cited by 3 publications

References 30 publications

The Rho kinase inhibitor Y-27632 increases erythrocyte deformability and low oxygen tension-induced ATP release

The Rho kinase inhibitor Y-27632 increases erythrocyte deformability and low oxygen tension-induced ATP release

Diamide decreases deformability of rabbit erythrocytes and attenuates low oxygen tension-induced ATP release

Differential In vitro and In vivo Behavior of Mouse Ascorbate/Fe3+ and Diamide Oxidized Erythrocytes

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