β -
thalassemia/Hb E is known to cause oxidative stress induced by
iron overload. The
glutathione system is the major
endogenous antioxidant that protects animal cells from oxidative damage. This study aimed to determine the effect of disease state and
splenectomy on redox status expressed by whole blood
glutathione (GSH)/
glutathione disulfide (
GSSG) and also to evaluate
glutathione-related responses to oxidation in β -
thalassemia/Hb E patients. Twenty-seven normal subjects and 25 β -
thalassemia/Hb E patients were recruited and blood was collected. The GSH/
GSSG ratio, activities of
glutathione-related
enzymes, hematological parameters, and serum
ferritin levels were determined in individuals. Patients had high
iron-induced oxidative stress, shown as significantly increased serum
ferritin, a decreased GSH/
GSSG ratio, and increased activities of
glutathione-related
enzymes.
Splenectomy increased serum
ferritin levels and decreased GSH levels concomitant with unchanged
glutathione-related
enzyme activities. The redox ratio had a positive correlation with
hemoglobin levels and negative correlation with levels of serum
ferritin. The
glutathione system may be the body's first-line defense used against oxidative stress and to maintain redox homeostasis in thalassemic patients based on the significant correlations between the GSH/GSSH ratio and degree of
anemia or body
iron stores.