Section of Experimental Pathology
Section of Experimental Pathology
Maria C.,Section of Experimental Pathology |
Pietro R.,Section of Experimental Pathology |
Mario V.,Messina University |
Isabella V.,Messina University |
Diana T.,Section of Experimental Pathology
Cell Biology International | Year: 2010
β-Thalassaemia is characterized by a decrease in globin β-chain synthesis and an excess in free α-globin chains. This induces alterations in membrane lipids and proteins resulting from a reduction in spectrin/band 3 ratio, partial oxidation of band 4.1 and clustering of band 3. The membrane injury provokes hyperhaemolysis and bone marrow hyperplasia. The pathophysiology of thalassaemia is associated with iron overload that generates oxygen free radicals and oxidative tissue injury with ocular vessel alterations. The aim of this research is to investigate the influence of oxidative stress on band 3 efficiency, which is an integral membrane protein of RBCs (red blood cells). Band 3 protein, of which there are more than 1 million copies per cell, is the most abundant membrane protein in human RBCs. It mediates the anion exchange and acid-base equilibrium through the RBC membrane. Some experiments were performed on thalassaemic cells and βthalassaemia-like cells and tested for sulfate uptake. To test the antioxidant effect of Mg2+, other experiments were performed using normal and pathological cells in the presence of Mg2+. The oxidant status in thalassaemic cells was verified by increased K+ efflux, by lower GSH levels and by increased G6PDH (glucose-6-phosphate dehydrogenase) activity. The rate constant of SO4 -2 uptake decreases in thalassaemic cells as well as in β-thalassaemia-like cells when compared with normal cells. It increases when both cells are incubated with Mg2+. Our data show that oxidative stress plays a relevant role in band 3 function of thalassaemic cells and that antioxidant treatment with Mg2+ could reduce oxidative damage to the RBC membrane and improve the anion transport efficiency regulated by band 3 protein. © The Author(s) Journal compilation © 2010 Portland Press Limited.
Venza I.,Azienda Ospedaliera Universitaria G. Martino |
Visalli M.,Section of Experimental Pathology |
Cucinotta M.,Section of Experimental Pathology |
Teti D.,Section of Experimental Pathology |
Venza M.,Azienda Ospedaliera Universitaria G. Martino
Aging Clinical and Experimental Research | Year: 2012
Background and aims: The aim of the present study was to determine whether age and gender affect the imbalance between oxidant production and antioxidant levels in age-related macular degeneration (ARMD) patients. Methods: Total superoxide dismutase (T-SOD), total glutathione peroxidase (T-GSHPx), and catalase (CAT) activities, as well as malondialdehyde (MDA), protein carbonyl (PC), 8-Hydroxy-29-deoxyguanosine (8-OHdG) and total oxidation status (TOS) levels, were measured in the following groups subdivided by age and gender: 156 early-ARMD patients; 80 wet-late ARMD patients; 72 dry-late ARMD patients; and 207 healthy controls. Results: Among all study participants, women aged 50-54 had higher T-SOD and T-GSHPx activities and lower MDA, PC, TOS and 8-OHdG levels than age-matched men (p<0.05), whereas older women were not significantly different from age-matched older men. Significantly increased oxidative damage was associated with ARMD patients >60 years of age in both sexes compared with controls (p<0.01 for 60-64 and 65-69-year-old ARMD sub-groups; p<0.001 for 70-74 and 75-80-year-old ARMD subgroups). Multiple regression analysis demonstrates that age significantly affects antioxidant status and oxidative damage in ARMD patients compared with controls (controls, p<0.05; ARMD patients, p<0.001). A direct correlation with antioxidant enzyme activities and an inverse correlation with oxidative DNA, protein and lipid damage were also observed in premenopausal women (controls, p<0.05; ARMD patients, p<0.001). Conclusions: Aging and postmenopausal status may be aggravating factors contributing to redox imbalance and oxidative damage in ARMD patients. ©2012, Editrice Kurtis.