Oxidative Stress and 𝜷-Thalassemic Erythroid Cells behind the Molecular Defect

Table 1

Effects of different antioxidant treatments in β thalassemia.

Molecule	Model	Evidences	Ref.
Vitamin E	β-thal intermedia patients (in vivo study)	↓ MDA; Amelioration in the oxidation of low density lipoproteins; Amelioration of RBCs osmotic fragility; No changes in transfusion requirement	[70–72]
Curcumin	β-thal patients; (in vitro study); β-thal/HbE patients; (in vivo study)	↓ lipid peroxidation; ↓ methemoglobin, but no changes in Hb levels	[73, 74]
FPP	β-thal major and intermedia patients; (in vitro study); β-thal/HbE patients; (in vivo study); β-thal mouse model; (in vivo)	↓ ROS; ↑ GSH; ↓ PS positive RBCs; ↓ RBCs phagocytosis; No effects on Hb levels	[73, 75]
MonoHER	β-thal mouse model; (in vivo)	↑ RBCs K^+ content; ↓ KCl cotransport activity; ↓ PS positive RBCs; ↑ RBCs membrane and plasma vitamin E levels; Amelioration of β-thal mouse erythropoiesis	[66]
AD4	β-thal major and intermedia patients; (in vitro study); β-thal mouse model; (in vivo study)	↓ ROS; ↑ GSH; ↓ PS positive RBCs; ↓ RBCs phagocytosis; No effects on Hb levels	[76]

β-thal: β-thalassemia; MDA: malonylaldehyde; RBC: red blood cell; Hb: hemoglobin; PS: phosphatidylserine; GSH: reduced glutathione peroxidase; ROS: reactive oxygen species; FPP: fermented papaya preparation; AD4: N-acetylcysteine amide.