scholarly journals Using Redox Potential as a Feasible Marker for Banked Blood Quality and the State of Oxidative Stress in Stored Red Blood Cells

2020 ◽  
Author(s):  
Rodney C Daniels ◽  
Hyesun Jun ◽  
Robertson D Davenport ◽  
Maryanne M Collinson ◽  
Kevin R Ward
Keyword(s):  
Oxidative Stress ◽  
Redox Potential ◽  
Red Blood Cells ◽  
Healthy Volunteers ◽  
Blood Cells ◽  
Storage Time ◽  
Cell Function ◽  
Venous Blood ◽  
Functional Changes ◽  
Over Time

Abstract Background Stored Red Blood Cells (RBCs) may undergo oxidative stress over time, with functional changes affecting critical tasks such as oxygen delivery. Central to these changes are oxidation-reduction (redox) reactions and the redox potential (RP) that must be maintained for proper cell function. RP imbalance can lead to oxidative stress that may contribute to storage lesions and transfusion-related morbidities. Direct measures of RP may allow for evaluation of erythrocyte quality and enable corrections of RP prior to transfusion. Methods Multiple random RBC segments were tested, ranging in age from 5 to 40 days at 5 day intervals. RP was recorded by measuring open circuit potential of RBCs using novel nanoporous gold electrodes with Ag/AgCl reference. RP measures were also performed on peripheral venous blood samples from 10 healthy volunteers. RP measures were compared between groups of aged RBCs, and with volunteer blood. Results Stored RBCs show time-dependent increases in RP. There were significant differences in Day 5 RP compared to all other groups (p≤0.005), Day 10-15 vs ages ≥ Day 20 (p≤0.025), Day 20-25 vs Day 40 (p=0.039), and all groups compared to healthy volunteers. RP became more positive over time suggesting ongoing oxidation as RBCs age. However, storage time alone does not predict the ultimate RP value measured from a given unit.Conclusions There are significant differences in RP between freshly stored RBCs and all others, with RP becoming more positive over time. However, storage time alone does not predict RP, indicating RP screening may be important independent of storage time and may serve as a marker of RBC quality and state of oxidative stress. RP measurements may also provide a target by which to restore RP balance in aged pRBCs, improving their clinical effectiveness while reducing associated morbidities.

scholarly journals Using redox potential as a feasible marker for banked blood quality and the state of oxidative stress in stored red blood cells

2021 ◽  
Author(s):  
Rodney C. Daniels ◽  
Hyesun Jun ◽  
Robertson D. Davenport ◽  
Maryanne M. Collinson ◽  
Kevin R. Ward
Keyword(s):  
Oxidative Stress ◽  
Redox Potential ◽  
Red Blood Cells ◽  
Blood Cells ◽  
The State

scholarly journals THE RATIO OF SYSTEMIC INFLAMMATION, OXIDATIVE STRESS AND GLUTATHIONE REDOX STATUS INDICATORS IN PATIENTS WITH CORONARY HEART DISEASE AND TYPE 2 DIABETES MELLITUS

2013 ◽  
Vol 19 (4) ◽  
pp. 356-366
Author(s):  
A. G. Moiseenok ◽  
I. V. Buko ◽  
I. V. Gorudko ◽  
E. E. Konstantinova ◽  
N. L. Tsapaeva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Coronary Heart Disease ◽  
Redox Potential ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Redox Status ◽  
Glutathione Redox

Objective. To study and compare indicators of systemic inlammation and red blood cells glutathione redox potential by chronic oxidative stress (OS) in patients with coronary heart disease (CHD), type 2 diabetes mellitus (T2DM) and the combination of both diseases.Design and methods. The study included 35 patients with CHD and newly diagnosed T2DM, 109 patients with CHD, 19 patients with T2DM, and 89 healthy individuals. Systemic inlammation indicators were measured including concentration of interleukin (IL) 6 and 8, myeloperoxidase (MPO) and OS in plasma, oxidized (GSSG) and reduced (GSH) glutathione, as well as their ratio and redox potential (E), the activity of glutathione reductase (GR) and glutathione peroxidase (GP) in red blood cells.Results. Signiicant growth of systemic inlammation (IL-6, IL-8, MPO) indicators on the weakening antioxidant defense enzyme has been registered in patients with a combination of CHD and T2DM, a 3,4-fold reduction of GSH level, 5,8-fold of 2GSH/GSSH in red blood cells and E values towards the oxidized state at 36,3 mV were noted. These changes were less pronounced in CHD group and were absent in T2DM group. All subjects showed a decreased activity of GP and increased level of glycosylated hemoglobin. The correlation of E and activity GR have been found in patients with carbohydrate metabolism disorder. High positive relationship between IL concentration and red blood cells GR, E indicators has been identiied in patients with CHD and T2DM. There is a need to control and correct cellular redox potential in patients with CHD and T2DM.Conclusion. The combination of CHD and T2DM contributes to the decrease of red blood cells redox status glutathione secondary to the increased systemic inlammatory response and chronic OS indicators.

Procoagulant Activity In Stored Units Of Red Blood Cells

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 1157-1157
Author(s):  
Saulius Butenas ◽  
Maya Aleshnick ◽  
Jonathan H Foley ◽  
Friederike K. Keating
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Storage Time ◽  
Conflicts Of Interest ◽  
Procoagulant Activity ◽  
Clotting Time ◽  
Autologous Plasma ◽  
Healthy Donors ◽  
Over Time ◽  
Corn Trypsin Inhibitor

Abstract It has been observed that the procoagulant activity of stored units of red blood cells (RBC) increases over time, which is, in part, related to the expression/exposure of tissue factor (TF) on blood cells and microparticles (Keating et al, Transfusion 2011;51:1086). However, in many instances there is a discrepancy between the levels of TF measured in stored units of RBC and changes in procoagulant activity observed over the storage time. We hypothesized that, in addition to TF, an exposure of an acidic phospholipid, phosphatidylserine (PS), on blood cells (Whelihan et al, Blood 2012;120:3837), could be the cause of an elevated procoagulant activity. Four healthy donors were recruited. RBC units were prepared and stored at 4°C for 30 days. On selected days, aliquots were removed, reconstituted with autologous plasma and recalcified, and were tested in the presence of corn trypsin inhibitor in the thromboelastography assay for procoagulant activity. For all 4 donors, the clotting time decreased from ∼3000-4000 s on day 1 to ∼1000-1600 s on day 30, with the most dramatic changes occurring between days 1 and 10. Addition of an inhibitory anti-TF antibody slightly prolonged clotting times, suggesting the presence of endogenous TF in RBC units. The concentration of TF, quantitated in an activity-based assay, did not change significantly over time for 3 of 4 donors and was within the range of 40-130 fM. For the fourth donor, TF concentration reached a maximum of 310 fM on day 10 and then decreased steadily to 60 fM on day 30. In an attempt to identify other components in RBC units responsible for the procoagulant activity, the effect of lactadherin, which binds to the phosphatidylserine exposed on cell membranes, was investigated. An addition of 100 nM lactadherin substantially prolonged the clotting time of the reconstituted RBC. Thus, in days 3-5 the clotting time in the presence of lactadherin was by 2.4-3.4-fold longer than in the absence of it. With increasing age of the RBC units, the effect of lactadherin diminished and at day 30, a prolongation of the clotting time did not exceed 1.3-1.8-fold. The addition of anti-TF monoclonal antibody in the presence of lactadherin further enhanced the clotting time of the reconstituted RBC. In conclusion, our data indicate that in stored units of RBC, the procoagulant activity is dependent upon the presence of active monocyte TF and phosphatidylserine exposed on blood cells and platelets. However, the failure of lactadherin in combination with the anti-TF antibody to completely inhibit the procoagulant activity in RBC units suggests that other components of blood (most likely platelets) support this activity as well. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Regulation of intracellular glutathione levels in erythrocytes infected with chloroquine-sensitive and chloroquine-resistant Plasmodium falciparum

2002 ◽  
Vol 368 (3) ◽  
pp. 761-768 ◽  
Author(s):  
Svenja MEIERJOHANN ◽  
Rolf D. WALTER ◽  
Sylke MÜLLER
Keyword(s):  
Oxidative Stress ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Differential Susceptibility ◽  
Protozoan Parasite ◽  
Chloroquine Resistance ◽  
Glutathione Metabolism ◽  
Glutathione Synthesis ◽  
Intracellular Glutathione ◽  
Glutamylcysteine Synthetase

Malaria is one of the most devastating tropical diseases despite the availability of numerous drugs acting against the protozoan parasite Plasmodium in its human host. However, the development of drug resistance renders most of the existing drugs useless. In the malaria parasite the tripeptide glutathione is not only involved in maintaining an adequate intracellular redox environment and protecting the cell against oxidative stress, but it has also been shown that it degrades non-polymerized ferriprotoporphyrin IX (FP IX) and is thus implicated in the development of chloroquine resistance. Glutathione levels in Plasmodium-infected red blood cells are regulated by glutathione synthesis, glutathione reduction and glutathione efflux. Therefore the effects of drugs that interfere with these metabolic processes were studied to establish possible differences in the regulation of the glutathione metabolism of a chloroquine-sensitive and a chloroquine-resistant strain of Plasmodiumfalciparum. Growth inhibition of P. falciparum 3D7 by d,l-buthionine-(S,R)sulphoximine (BSO), an inhibitor of γ-glutamylcysteine synthetase (γ-GCS), and by Methylene Blue (MB), an inhibitor of gluta thione reductase (GR), was significantly more pronounced than inhibition of P.falciparum Dd2 growth by these drugs. These results correlate with the higher levels of total glutathione in P. falciparum Dd2. Short-term incubations of Percoll-enriched trophozoite-infected red blood cells in the presence of BSO, MB and N,N1-bis(2-chloroethyl)-N-nitrosourea and subsequent determinations of γ-GCS activities, GR activities and glutathione disulphide efflux revealed that maintenance of intracellular glutathione in P. falciparum Dd2 is mainly dependent on glutathione synthesis whereas in P. falciparum 3D7 it is regulated via GR. Generally, P. falciparum Dd2 appears to be able to sustain its intracellular glutathione more efficiently than P. falciparum 3D7. In agreement with these findings is the differential susceptibility to oxidative stress of both parasite strains elicited by the glucose/glucose oxidase system.

Redox imbalance of red blood cells impacts T lymphocyte homeostasis: implication in carotid atherosclerosis

2011 ◽  
Vol 106 (12) ◽  
pp. 1117-1126. ◽  
Author(s):  
Brigitta Buttari ◽  
Linda Petrone ◽  
Elisabetta Straface ◽  
Lucrezia Gambardella ◽  
Donatella Pietraforte ◽  
...  
Keyword(s):  
T Cell ◽  
T Lymphocytes ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Healthy Subjects ◽  
Carotid Atherosclerosis ◽  
Cell Function ◽  
Inflammatory Responses ◽  
Activated T Lymphocytes

SummaryOxidative stress and immune/inflammatory responses are key pathogenetic factors of atherosclerotic disease. In this contest, mechanisms that regulate survival and death of immune cells may be relevant. Previous studies have demonstrated that red blood cells (RBCs) are physiologically able to inhibit apoptosis and to promote proliferation of activated T lymphocytes from healthy subjects. The aim of the present study was to evaluate whether RBCs from patients with carotid atherosclerosis maintain their property to modulate T cell homeostasis. Peripheral blood lymphocytes (PBLs) obtained from healthy subjects were activated in vitro by phytohemagglutinin in the presence/absence of RBCs from patients with carotid atherosclerosis or of in vitro oxidised RBCs from healthy subjects. Levels of reactive oxygen species (ROS) and aging markers of RBCs as well as susceptibility to apoptosis of PBLs were evaluated by flow cytometry. PBL proliferation was evaluated by 3H-methyl-thymidine incorporation assay whereas secretion of cytokines, analysed in view of their key role in T cell function, was assessed by ELISA. Levels of ROS and phosphatidyl-serine externalisation, a sign of RBC aging, resulted significantly higher in RBCs from patients than in those from healthy subjects, whereas surface glycophorin A expression and reduced glutathione content did the opposite. Unlike RBCs obtained from healthy subjects, RBCs from patients and in vitro oxidised RBCs did not protect activated T lymphocytes from apoptosis. Hence, RBCs from patients with carotid atherosclerosis, probably due to their oxidative imbalance, impact T cell integrity and function. Our results suggest a new regulatory role for RBCs in atherosclerosis.

scholarly journals Effect of aspartame on biochemical and oxidative stress parameters in rat blood

2015 ◽  
Vol 67 (2) ◽  
pp. 535-545 ◽  
Author(s):  
Marko Prokic ◽  
Milica Paunovic ◽  
Milos Matic ◽  
Natasa Djordjevic ◽  
Branka Ognjanovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Biochemical Parameters ◽  
White Blood Cells ◽  
Lipid Peroxides ◽  
Hdl Cholesterol ◽  
Albino Rats ◽  
Total Body Mass ◽  
Antioxidative Status

Aspartame (ASP) is one of the most widely used nonnutritive sweeteners. This study investigates the chronic effects of ASP on hematological and biochemical parameters, and its effects on the oxidative/antioxidative status in the red blood cells of Wistar albino rats. Rats were provided with ASP (40 mg/kg/daily for six weeks) in drinking water. Increased food and fluid intake was observed in the ASP-treated rats. Total body mass was significantly decreased in the ASP-treated rats. Treatment with ASP caused an increase in the concentrations of glucose, cholesterol, LDL-cholesterol, and in the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH), as well as a decrease in the levels of HDL-cholesterol in the serum. A significant decline in the number of white blood cells (WBC) was observed after ASP uptake. Based on the results we conclude that ASP induces oxidative stress, observed as an alteration of the glutathione redox status, which leads to increased concentrations of nitric oxide (NO) and lipid peroxides (LPO) in the red blood cells. Changes in biochemical parameters, lipid metabolism, as well as changes in the levels of oxidative stress markers and the appearance of signs of liver damage indicate that chronic use of ASP can lead to the development of hyperglycemia, hypercholesterolemia and associated diseases.

scholarly journals Crosstalk between Red Blood Cells and the Immune System and Its Impact on Atherosclerosis

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Brigitta Buttari ◽  
Elisabetta Profumo ◽  
Rachele Riganò
Keyword(s):  
Oxidative Stress ◽  
Immune System ◽  
Red Blood Cells ◽  
Immune Cells ◽  
Blood Cells ◽  
Atherosclerotic Disease ◽  
Intraplaque Hemorrhage ◽  
Immune System Activation ◽  
Adaptive Immune Cells ◽  
The Impact

Atherosclerosis is a chronic multifactorial disease of the arterial wall characterized by inflammation, oxidative stress, and immune system activation. Evidence exists on a pathogenic role of oxidized red blood cells (RBCs) accumulated in the lesion after intraplaque hemorrhage. This review reports current knowledge on the impact of oxidative stress in RBC modifications with the surface appearance of senescent signals characterized by reduced expression of CD47 and glycophorin A and higher externalization of phosphatidylserine. The review summarizes findings indicating that oxidized, senescent, or stored RBCs, due to surface antigen modification and release of prooxidant and proinflammatory molecules, exert an impaired modulatory activity on innate and adaptive immune cells and how this activity contributes to atherosclerotic disease. In particular RBCs from patients with atherosclerosis, unlike those from healthy subjects, fail to control lipopolysaccharide-induced DC maturation and T lymphocyte apoptosis. Stored RBCs, accompanied by shedding of extracellular vesicles, stimulate peripheral blood mononuclear cells to release proinflammatory cytokines, augment mitogen-driven T cell proliferation, and polarize macrophages toward the proinflammatory M1 activation pathway. Collectively, literature data suggest that the crosstalk between RBCs with immune cells represents a novel mechanism by which oxidative stress can contribute to atherosclerotic disease progression and may be exploited for therapeutic interventions.

Sign in / Sign up

Export Citation Format

Share Document