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anemia/antioxidante
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Antioxidant status of Fanconi anemia fibroblasts.
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Several observations in the recent literature have indicated that Fanconi anemia (FA) cells may be primarily deficient in the detoxification of activated oxygen species. To evaluate the antioxidant status of FA fibroblasts, we measured Mn-containing superoxide dismutase (Mn-SOD), CuZn-containing
Iron deficiency anemia and total antioxidant capacity.
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Oxidative stress in anemia.
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The increased formation of reactive oxygen species under hypoxic conditions often appears paradoxical. A prooxidant shift results from changes in cellular metabolism (especially energy metabolism), higher flux rates in catecholamine metabolism and permanent leukocyte activation. These mechanisms of
Natural antioxidant therapy for patients with hemolytic anemia.
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[Prevention of myocardial damage during hemolytic anemia by antioxidants].
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Structural and functional disorders of the heart muscle were studied in rats with phenylhydrazine-induced chronic hemolytic anemia, as was the possibility of their prevention with anti-oxidant Ionol, a lipid peroxidation inhibitor. Hemolytic anemia was shown to produce myocardial contractural
Interaction of antioxidants and their implication in genetic anemia.
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The generation of reactive oxygen species (ROS) is a steady-state cellular event in respiring cells. Their production can be grossly amplified in response to a variety of pathophysiological conditions such as inflammation, immunologic disorders, hypoxia, hyperoxia, metabolism of drug or alcohol,
Copper deficiency anemia: review article.
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Copper is a crucial micronutrient needed by animals and humans for proper organ function and metabolic processes such as hemoglobin synthesis, as a neurotransmitter, for iron oxidation, cellular respiration, and antioxidant defense peptide amidation, and in the formation of pigments and connective
[Antioxidant enzyme activity of the erythrocytes in anemia in children].
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Theoretical prerequisites have been submitted for possible alteration in the activity of erythrocytic antioxidant enzymes in children with anemia. The results are presented of the investigation of children with varying anemias for activity of erythrocytic superoxide dismutase and catalase.
Erythrocyte Catalase Activity in More Frequent Microcytic Hypochromic Anemia: Beta-Thalassemia Trait and Iron Deficiency Anemia.
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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
Oxidative status in iron-deficiency anemia.
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Oxidative stress is an imbalance between free radicals and antioxidant molecules that can play an important role in the pathogenesis of iron-deficiency anemia (IDA). The aim of this study was to investigate oxidative status in patients with IDA and alteration of oxidative status after iron
[The antioxidant effects of emoxipin in patients with iron-deficiency anemia].
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A total of 78 female patients of child-bearing age with iron deficiency anemia (IDA) of varying genesis and degree of severity were examined for effectiveness of a synthetic antioxidant emoxypine in a combined treatment of IDA. IDA was found to be associated with activation of lipid peroxidation
Blood antioxidant parameters in sickle cell anemia patients in steady state.
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Sickle cell anemia (SCA) is a hereditary disorder with higher potential for oxidative damage due to chronic redox imbalance in red cells. We measured antioxidant enzymes including catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD). We also determined oxidative damage of
[Effects of oxidants and antioxidants on chromosome breaks in Fanconi's anemia].
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[Myocardium damage in experimental anemia and its prevention with the antioxidant ionol].
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Rats with hemolytic (phenylhydrazine) anemia were shown to develop simultaneously with hypertrophy of the myocardium marked damages of cardiomyocytes of the type of I-III degree contractures, myocytolysis, vacuolation, fatty infiltration, small focal necrosis as well as a peculiar form of damages
Zinc and antioxidant vitamin deficiency in patients with severe sickle cell anemia.
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BACKGROUND
Patients with severe sickle cell anemia (SCA) have a higher potential for oxidative damage due to chronic redox imbalance in red blood cells that often leads to hemolysis, endothelial injury and recurrent vaso-occlusive episodes. This study evaluated the plasma levels of vitamins A, C and
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