Oxidative stress-dependent oligomeric status of erythrocyte peroxiredoxin II (PrxII) during storage under standard blood banking conditions

Rinalducci, Sara; D’Amici, Gian Maria; Blasi, Barbara; Zolla, Lello

doi:10.1016/j.biochi.2011.02.005

Cited by 32 publications

(27 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For this reason, a proteomic approach using MS was employed to verify if the temporary inactivation observed for this enzyme after 21 days of blood storage was due to an oxidation of this active‐site cysteine. To this end, in this set of experiments a thiol‐blocking agent ( N ‐ethylmaleimide) was used before sample preparation to lock any possible GAPDH redox forms, so as to avoid artifacts of oxidation upon RBC lysis and extract preparation . Membranes and cytosol of stored RBC were then analyzed by reduced and nonreduced Western blotting using antibodies to GAPDH.…”

Section: Resultsmentioning

confidence: 99%

Thiol‐based regulation of glyceraldehyde‐3‐phosphate dehydrogenase in blood bank–stored red blood cells: a strategy to counteract oxidative stress

2014

Self Cite

View full text Add to dashboard Cite

show abstract

Section: Resultsmentioning

confidence: 99%

Thiol‐based regulation of glyceraldehyde‐3‐phosphate dehydrogenase in blood bank–stored red blood cells: a strategy to counteract oxidative stress

2014

Self Cite

View full text Add to dashboard Cite

show abstract

“…Since a functioning SAM cycle is required for both GSH synthesis and cellular methylation reactions (Figures 3 and 5) [44], it was surprising to observe a block in this cycle during storage that disrupted homocysteine remethylation to methionine, thus preventing regeneration of SAM. This metabolic defect was previously unrecognized in stored RBCs.…”

Section: Discussionmentioning

confidence: 99%

“…Based on current regulations, RBC units collected for transfusion may be stored up to 42 days at refrigerated temperature prior to infusion. There is extensive evidence that RBCs undergo changes in proteins, lipids and other cellular constituents during storage [1–5]. Additionally, recent clinical studies indicate that patients infused with RBC units stored for longer pre-transfusion periods have worse clinical outcomes than do patients transfused relatively fresher units [6–8].…”

Section: Introductionmentioning

confidence: 99%

Metabolomics of ADSOL (AS-1) Red Blood Cell Storage

Roback

Josephson

Waller

et al. 2014

Transfusion Medicine Reviews

109

View full text Add to dashboard Cite

Background Population based investigations suggest that red blood cells (RBCs) are therapeutically effective when collected, processed and stored for up to 42 days under validated conditions prior to transfusion. However, some retrospective clinical studies have shown worse patient outcomes when transfused RBCs have been stored for the longest times. Furthermore, studies of RBC persistence in the circulation after transfusion have suggested that considerable donor-to-donor variability exists, and may affect transfusion efficacy. To understand the limitations of current blood storage technologies and to develop approaches to improve RBC storage and transfusion efficacy, we investigated the global metabolic alterations that occur when RBCs are stored in AS-1 (AS1-RBC). Methods Leukoreduced AS1-RBC units prepared from 9 volunteer research donors (12 total donated units) were serially sampled for metabolomics analysis over 42 days of refrigerated storage. Samples were tested by GC/MS and LC/MS/MS, and specific biochemical compounds were identified by comparison to a library of purified standards. Results Over three experiments, 185–264 defined metabolites were quantified in stored RBC samples. Kinetic changes in these biochemicals confirmed known alterations in glycolysis and other pathways previously identified in RBCs stored in SAGM (SAGM-RBC). Furthermore, we identified additional alterations not previously seen in SAGM-RBCs (e.g., stable pentose phosphate pathway flux, progressive decreases in oxidized glutathione), and we delineated changes occurring in other metabolic pathways not previously studied (e.g., S-adenosyl methionine cycle). These data are presented in the context of a detailed comparison with previous studies of SAGM-RBCs from human donors and murine AS1-RBCs. Conclusion Global metabolic profiling of AS1-RBCs revealed a number of biochemical alterations in stored blood that may affect RBC viability during storage as well as therapeutic effectiveness of stored RBCs in transfusion recipients. Significance These results provide future opportunities to more clearly pinpoint the metabolic defects during RBC storage, to identify biomarkers for donor screening and prerelease RBC testing, and to develop improved RBC storage solutions and methodologies.

show abstract

“…Specific proposed mechanisms of injury include increased oxidative stress and inflammation, inhibition of nitric oxide (NO) signaling and perturbation of iron homeostasis. Mediating this gain of toxicity are several storage‐dependent changes to the RBCs that include formation of smaller and more dense cells (that display increased rates of NO and nitrite oxidation), release of microparticles, hemolysis, and release of free hemoglobin (Hb) and free heme (hemin), loss of ATP, and increased levels of products from oxidative stress …”

mentioning

confidence: 99%

Predicting storage‐dependent damage to red blood cells using nitrite oxidation kinetics, peroxiredoxin‐2 oxidation, and hemoglobin and free heme measurements

Oh¹,

Stapley²,

Harper³

et al. 2015

Transfusion

View full text Add to dashboard Cite

Background Storage-dependent damage to RBCs varies significantly. Identifying RBC units that will undergo higher levels of hemolysis during storage may allow for more efficient inventory management decision-making. Oxidative-stress mediates storage-dependent damage to RBCs and will depend on the oxidant : antioxidant balance. We reasoned that this balance or redox tone will serve as a determinant of how a given RBC unit stores and that its assessment in “young” RBC will predict storage-dependent hemolysis. Study Design and Methods RBCs were sampled from bags and segments stored for 7d – 42d. Redox tone was assessed by nitrite oxidation kinetics and peroxiredoxin-2 (Prx-2) oxidation. In parallel, hemolysis was assessed by measuring cell-free hemoglobin and free-heme (hemin). Correlation analyses were performed to determine if d7 measurements predicted either the level of hemolysis at d35 or the increase in hemolysis during storage. Results Higher d7 Prx-2 oxidation was associated with higher d35 Prx-2 oxidation suggesting that early assessment of this parameter may identify RBCs that will incur the most oxidative damage during storage. RBCs that oxidized nitrite faster at d7 were associated with greatest levels of storage-dependent hemolysis and increases in Prx-2 oxidation. An inverse relationship between storage-dependent changes in oxyhemoglobin and free heme was observed underscoring an unappreciated reciprocity between these molecular species. Moreover, free heme was higher in the bag compared to paired segments, with opposite trends observed for free hemoglobin. Conclusion Measurement of Prx-2 oxidation, nitrite oxidation kinetics early during RBC storage may predict storage-dependent damage to RBC including hemolysis-dependent formation of free hemoglobin and heme.

show abstract

Oxidative stress-dependent oligomeric status of erythrocyte peroxiredoxin II (PrxII) during storage under standard blood banking conditions

Cited by 32 publications

References 51 publications

Thiol‐based regulation of glyceraldehyde‐3‐phosphate dehydrogenase in blood bank–stored red blood cells: a strategy to counteract oxidative stress

Thiol‐based regulation of glyceraldehyde‐3‐phosphate dehydrogenase in blood bank–stored red blood cells: a strategy to counteract oxidative stress

Metabolomics of ADSOL (AS-1) Red Blood Cell Storage

Predicting storage‐dependent damage to red blood cells using nitrite oxidation kinetics, peroxiredoxin‐2 oxidation, and hemoglobin and free heme measurements

Contact Info

Product

Resources

About