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Antioxid Redox Signal 2011 May 1;14(9):1713-28

Blood aging, safety and transfusion: capturing the "radical" menace.

Buehler PW, Karnaukhova E, Gelderman MP, Alayash AI

Abstract

Throughout their life span, circulating red blood cells (RBCs) transport oxygen (O2) primarily from the lungs to tissues and return with carbon dioxide (CO2) from respiring tissues for final elimination by lungs. This simplistic view of RBCs as O2 transporter has changed in recent years as other gases, e.g., nitric oxide, (NO) and small molecules e.g., adenosine triphosphate, (ATP) have been shown to either be produced and/or carried by RBCs to perform other signaling and O2 sensing functions. In spite of the numerous biochemical and metabolic changes occurring within RBCs during storage, prior to and after transfusion, perturbations of RBC membrane are likely to affect blood flow in the microcirculation. Subsequent hemolysis due to storage conditions and/or hemolytic disorders may have some pathophysiological consequences as a result of the release of Hb. In this review, we show that evolution has provided a multitude of protection and intervention strategies against free Hb from "cradle" to "death"; from early biosynthesis to its final degradation and a lot more in between. Furthermore, some of the same naturally occurring protective mechanisms can potentially be employed to oxidatively inactivate this redox active protein and control its damaging side reactions when released outside of the RBC.


Category: Journal Article
PubMed ID: #20954814 DOI: 10.1089/ars.2010.3447
Includes FDA Authors from Scientific Area(s): Biologics
Entry Created: 2011-10-03 Entry Last Modified: 2012-08-29
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