info:eu-repo/semantics/article
Genetic Regulation of Redox Balance in β-Thalassemia Trait
Fecha
2020-03Registro en:
Teran, Magdalena María; Mónaco, María Elvira; Lazarte, Sandra Stella; Haro, Ana Cecilia; Ledesma, Achem Emilse; et al.; Genetic Regulation of Redox Balance in β-Thalassemia Trait; Taylor & Francis; Hemoglobin; 44; 2; 3-2020; 122-127
0363-0269
CONICET Digital
CONICET
Autor
Teran, Magdalena María
Mónaco, María Elvira
Lazarte, Sandra Stella
Haro, Ana Cecilia
Ledesma, Achem Emilse
Alvarez Asensio, Natalia Sofía
Isse, Blanca Alicia de Los Angeles G.
Resumen
β-Thalassemia (β-thal) trait is a heterogeneous group of genetic defects leading to decreased β-globin production, ineffective erythropoiesis, and oxidative stress. The aim is to evaluate the cytoprotective response, at transcriptional and systemic levels, of the variations of global redox balance in β-thal trait patients. Sixty-six subjects (40 healthy and 26 with β-thal trait) were analyzed at the Universidad Nacional de Tucumán, Tucumán, Argentina, between 2016 and 2017. The following parameters were evaluated: complete blood count, iron status, hemoglobin (Hb) electrophoresis, Hb A2, thiobarbituric acid reactive species (TBARS), serum catalase (CAT), and superoxide dismutase (SOD) activity, FOXO3a, NRF2, SOD, PRDX2, CAT, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) gene expression. The β-thal trait group showed a decrease in Hb levels, MCV, and MCH with higher TBARS levels. The SOD activity was significantly increased by 32.0% in β-thal trait patients respect to the control group. Relative expression of NRF2 was 4.7-fold higher in β-thal trait than in the control group, while FOXO3a expression was similar in both groups. The SOD, PRDX2, and proinflammatory cytokines transcriptional expression was significantly upregulated in β-thal trait patients. This is the first study on the genetic regulation of redox balance in β-thal trait patients in which interesting modifications were observed in the transcript levels of some redox regulators that could be associated with changes in the erythrocyte proteome in this disorder. A better understanding of the pathophysiological mechanisms present in these heterozygous patients would allow adequate therapy in situations such as growth, pregnancy, or high performance sports, favoring a personalized treatment.