Genetic Regulation of Redox Balance in β-Thalassemia Trait.

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.

Foxo3 gene expression and oxidative status in beta-thalassemia minor subjects.

Background: Oxidative stress may aggravate symptoms of hemolytic anemias such as beta-thalassemia. FoxO3 activation results in resistance to oxidative stress in fibroblasts and neuronal cell cultures.

Objective: The purpose of this research was to study FoxO3 gene expression and oxidative status in beta-thalassemia minor individuals.

Erythrocyte Catalase Activity in More Frequent Microcytic Hypochromic Anemia: Beta-Thalassemia Trait and Iron Deficiency Anemia.

Most common microcytic hypochromic anemias are iron deficiency anemia (IDA) and β-thalassemia trait (BTT), in which oxidative stress (OxS) has an essential role. Catalase causes detoxification of H2O2 in cells, and it is an indispensable antioxidant enzyme. The study was designed to measure erythrocyte catalase activity (ECAT) in patients with IDA (10) or BTT (21), to relate it with thalassemia mutation type (β (0) or β (+)) and to compare it with normal subjects (67).