Antioxidant defence of red blood cells and plasma in stored human blood

Jóźwik, Maciej; Jóźwik, Marcin; Szczypka, M; Gajewska, Joanna; Laskowska-Klita, Teresa

doi:10.1016/s0009-8981(97)00148-4

Cited by 60 publications

(32 citation statements)

References 48 publications

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“…The concentration and stability of these metabolites during the storage of RBCs has been associated with the RBC storage lesion [13, 17, 19, 43, 44]. Supplementation of stored RBCs with GSH has been shown to partially protect from free radical and oxidant-induced injury, thereby maintaining more normal cellular function [12, 16].…”

Section: Discussionmentioning

confidence: 99%

Heritability of glutathione and related metabolites in stored red blood cells

Erve

Doskey

Wagner

et al. 2014

Free Radical Biology and Medicine

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Red blood cells (RBCs) collected for transfusion deteriorate during storage. This deterioration is termed the “RBC storage lesion”. There is increasing concern over the safety, therapeutic efficacy, and toxicity of transfusing longer-stored units of blood. The severity of the RBC storage lesion is dependent on storage-time and varies markedly between individuals. Oxidative damage is considered a significant factor in development of the RBC storage lesion. In this study, the variability during storage and heritability of antioxidants and metabolites central to RBC integrity and function were investigated. In a classic twin study, we determined the heritability of glutathione (GSH), glutathione disulfide (GSSG), the status of the GSSG, 2H+/2GSH couple (Ehc) and total glutathione (tGSH) in donated RBCs over 56 days of storage. Intracellular GSH and GSSG concentrations both decrease during storage (median net loss of 0.52 ± 0.63 mM (median ± SD) and 0.032 ± 0.107mM, respectively over 42 days). Taking into account the decline in pH, Ehc became more positive (oxidized) during storage (median net increase of 35 ± 16 mV). In our study population heritability estimates for GSH, GSSG, tGSH, and Ehc measured over 56 days of storage are 79%, 60%, 67%, and, 75% respectively. We conclude that susceptibility of stored RBCs to oxidative injury due to variations in the GSH-redox buffer are highly variable among individual donors and strongly heritable. Identifying the genes that regulate the storage-related changes in this redox buffer could lead to the development of new methods to minimize the RBC storage lesion.

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Section: Discussionmentioning

confidence: 99%

Heritability of glutathione and related metabolites in stored red blood cells

Erve

Doskey

Wagner

et al. 2014

Free Radical Biology and Medicine

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“…It has been proposed that several biochemical changes and depletion in the antioxidant defense system occur on storage of G6PD-deficient blood. [89] In infants, Mimouni et al , described hemolysis in 2 preterm infants who received G6PD-deficient donor blood. Neither infant received drugs known to be hemolytic.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of glucose-6-phosphate dehydrogenase deficiency and sickle cell trait among blood donors in Riyadh

Alabdulaali

Alayed

Alshaikh

et al. 2010

Asian J Transfus Sci

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Background and Aims:Blood donation from glucose-6-phosphate dehydrogenase (G6PD)-deficient and sickle cell trait (SCT) donors might alter the quality of the donated blood during processing, storage or in the recipient's circulatory system. The aim of this study was to determine the prevalence of G6PD deficiency and SCT among blood donors coming to King Khalid University Hospital (KKUH) in Riyadh. It was also reviewed the benefits and risks of transfusing blood from these blood donors.Materials and Methods:This cross-sectional study was conducted on 1150 blood samples obtained from blood donors that presented to KKUH blood bank during the period April 2006 to May 2006. All samples were tested for Hb-S by solubility test, alkaline gel electrophoresis; and for G6PD deficiency, by fluorescent spot test.Results:Out of the 1150 donors, 23 (2%) were diagnosed for SCT, 9 (0.78%) for G6PD deficiency and 4 (0.35%) for both conditions. Our prevalence of SCT and G6PD deficiency is higher than that of the general population of Riyadh.Conclusion:We recommend to screen all units for G6PD deficiency and sickle cell trait and to defer donations from donors with either of these conditions, unless if needed for special blood group compatibility, platelet apheresis or if these are likely to affect the blood bank inventory. If such blood is to be used, special precautions need to be undertaken to avoid complications in high-risk recipients.

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“…Cell senescence and changes in RBC reducing power (i.e. depletion of endogenous antioxidants) can accelerate the rate of Hb autoxidation and elevate the concentration of intracellular ROS [68]. Another concern is the level of molecular oxygen within the RBC unit that is available for redox reactions [69,70].…”

Section: Factors Promoting Hb Oxidation During Ex Vivo Storage Of Rbcsmentioning

confidence: 99%

“…Changes in RBC reducing power during hypothermic storage have been primarily attributed to the exhaustion of GSH and its related enzymes, including glutathione reductase and glutathione peroxidase [74]. Significant reductions in the RBC GSH content (30%) and glutathione reductase (8%) have been observed after 25 days of storage in citrate–phosphate–dextrose–adenine storage solution [68]. A similar study reported ∼ 30% depletion of glutathione reductase and glutathione peroxidase after 35 days of preservation in adenine–dextrose–sodium chloride–mannitol storage solution (ADSOL) [75].…”

Section: Factors Promoting Hb Oxidation During Ex Vivo Storage Of Rbcsmentioning

confidence: 99%

Biopreservation of red blood cells – the struggle with hemoglobin oxidation

2010

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One of the least recognized causes of cellular damage during ex vivo preservation of red blood cells is oxidative injury to the hemoglobin. The latter has been associated with hemolysis through the release of toxic substances and oxidation of vital cell components. This review delineates some of the major pathways that link hemoglobin oxidation and cellular damage, and summarizes the incidence of red blood cell oxidative injury during hypothermic storage, cryopreservation and desiccation stress. Red blood cell hypothermic storage, despite its success, is not exempt from oxidative injury. Growing evidence portrays a time‐dependant oxidative assault including formation of reactive oxygen species, attachment of denatured hemoglobin to membrane phospholipids and the release of hemoglobin‐containing membrane microvesicles throughout storage. Similar symptoms have been observed in attempts to stabilize red blood cells in the dried state, in which methemoglobin levels of reconstituted red blood cells reached 50%. Factors affecting the rate of hemoglobin oxidation during red blood cell ex vivo storage include compromised antioxidant activity, high concentrations of glucose in the storage media and the presence of molecular oxygen. Hemoglobin oxidation largely dictates our ability to effectively preserve red blood cells. Understanding its origins along with investigating methods to minimize it can significantly improve the quality of our future blood products.

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Antioxidant defence of red blood cells and plasma in stored human blood

Cited by 60 publications

References 48 publications

Heritability of glutathione and related metabolites in stored red blood cells

Heritability of glutathione and related metabolites in stored red blood cells

Prevalence of glucose-6-phosphate dehydrogenase deficiency and sickle cell trait among blood donors in Riyadh

Biopreservation of red blood cells – the struggle with hemoglobin oxidation

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