| Texto completo | |
| Autor(es): |
Humberto Silva, Danilo Grunig
[1, 2]
;
Belini Junior, Edis
[1]
;
de Almeida, Eduardo Alves
[2]
;
Bonini-Domingos, Claudia Regina
[1]
Número total de Autores: 4
|
| Afiliação do(s) autor(es): | [1] Sao Paulo State Univ Julio de Mesquita Filho, Dept Biol, Hemoglobin & Hematol Genet Dis Lab, BR-15054000 Sao Jose Do Rio Preto, SP - Brazil
[2] Sao Paulo State Univ Julio de Mesquita Filho, Dept Chem & Environm Sci, Lab Aquat Contaminat Biomarkers, BR-15054000 Sao Jose Do Rio Preto, SP - Brazil
Número total de Afiliações: 2
|
| Tipo de documento: | Artigo de Revisão |
| Fonte: | Free Radical Biology and Medicine; v. 65, p. 1101-1109, DEC 2013. |
| Citações Web of Science: | 38 |
| Resumo | |
Erythrocytes have an environment of continuous pro-oxidant generation due to the presence of hemoglobin (Hb), which represents an additional and quantitatively significant source of superoxide (O-2(center dot-)) generation in biological systems. To counteract oxidative stress, erythrocytes have a self-sustaining antioxidant defense system. Thus, red blood cells uniquely function to protect Hb via a selective barrier allowing gaseous and other ligand transport as well as providing antioxidant protection not only to themselves but also to other tissues and organs in the body. Sickle hemoglobin molecules suffer repeated polymerization/depolymerization generating greater amounts of reactive oxygen species, which can lead to a cyclic cascade characterized by blood cell adhesion, hemolysis, vaso-occlusion, and ischemia-reperfusion injury. In other words, sickle cell disease is intimately linked to a pathophysiologic condition of multiple sources of pro-oxidant processes with consequent chronic and systemic oxidative stress. For this reason, newer therapeutic agents that can target oxidative stress may constitute a valuable means for preventing or delaying the development of organ complications. (C) 2013 Elsevier Inc. All rights reserved. (AU) | |