NTPDase, 5′-nucleotidase and adenosine deaminase activities and purine levels in serum of sickle cell anemia patients

• Autor(a) principal: Castilhos, Lívia Gelain
• Data de Publicação: 2018
• Outros Autores: Adefegha, Stephen A., Doleski, Pedro Henrique, Bertoldo, Tatiana Montagner Dalcin, Moritz, César Eduardo Jacintho, Casali, Emerson Andre, Leal, Daniela Bitencourt Rosa
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFRGS
• Texto Completo: http://hdl.handle.net/10183/182693
• topic: Purinérgicos; Adenosina desaminase; Soro; Anemia falciforme; NTPDase; 50-nucleotidase; Adenosine deaminase; Serum; Sickle cell anemia

Sickle cell anemia (SCA) is a hereditary disorder that is characterized by tendency of hemoglobin molecules within the erythrocytes to polymerize under hypoxia conditions, deform the red cells, and promote vaso-occlusion and endothelial damage. This disease may be associated with the extracellular release of nucleotides, particularly ATP, ADP and adenosine into the circulation. The aim of this study was to investigate the possible changes in adenine nucleotides and nucleoside metabolizing enzymes as well as their levels in serum of SCA patients. NTPDase, 50-nucleotidase and adenosine deaminase activities were evaluated in serum obtained from blood samples of 15 SCA treated patients and 15 healthy subjects (control group). The results revealed that there were significant (P < 0.001) elevations in NTPDase, 50-nucleotidase and ADA activities in serum of SCA treated patients when compared to the control group. Furthermore, no significant (P > 0.05) alteration was observed in ATP, ADP and adenosine levels of both SCA treated and control groups. However, inosine level was significantly (P < 0.05) decreased and hypoxanthine level was higher in SCA treated patients (P < 0.001) when compared to the control group. The results suggest the involvement of purinergic signaling enzymes in the maintenance of the levels of extracellular nucleotides and nucleosides, thus preventing some pathophysiological conditions associated with SCA.