The Role of Oxidative Stress in Hemolytic Anemia

Abstract

The oxidative status of cells is determined by the balance between pro-oxidants and antioxidants. Pro-oxidants, referred to as reactive oxygen species (ROS), are classified into radicals and nonradicals. The radicals are highly reactive due to their tendency to accept or donate an electron and attain stability. When cells experience oxidative stress, ROS, which are generated in excess, may oxidize proteins, lipids and DNA - leading to cell death and organ damage. Oxidative stress is believed to aggravate the symptoms of many diseases, including hemolytic anemias. Oxidative stress was found in the beta-hemoglobinopathies (sickle cell anemia and thalassemia), glucose-6-phosphate dehydrogenase deficiency, hereditary spherocytosis, congenital dyserythropoietic anaemias and Paroxysmal Nocturnal Hemoglobinuria. Although oxidative stress is not the primary etiology of these diseases, oxidative damage to their erythroid cells plays a crucial role in hemolysis due to ineffective erythropoiesis in the bone marrow and short survival of red blood cells (RBC) in the circulation. Moreover, platelets and polymorphonuclear (PMN) white cells are also exposed to oxidative stress. As a result some patients develop thromboembolic phenomena and recurrent bacterial infections in addition to the chronic anemia. In this review we describe the role of oxidative stress and the potential therapeutic potential of anti-oxidants in various hemolytic anemias.

Physiologically aged red blood cells undergo erythrophagocytosis in vivo but not in vitro

“…The results ( Figure 5B) showed that both kinds of cultured macrophages failed to phagocytose sRBC from either ht-or control-mice. However, in agreement with previous studies, 8,17,20,68 cultured macrophages phagocytosed RBC that have been used to provide a model for sRBC through treatments that induce overexpression of a single senescence property. Thus, while naturally aged RBC exposing moderate PS levels were not phagocytosed in vitro, substantial induction of PS externalization by treatment of control RBC with a calcium-ionophore led to significant EPC in vitro (Figures 2A and 5A).…”

Oxidative stress and antioxidative parameters in patients with spinal cord injury: implications in the pathogenesis of disease

“…Oxidative stress and generation of free radicals, as primary or secondary event, have been related in a great number of diseases. 9 Like ROS, reactive nitrogen species could also have a significant role in the pathogenesis of many diseases, and have drawn significant attention in recent years. Nitric oxide (NO), generated by the enzyme inducible NO synthase, is one of the most important and widely studied reactive nitrogen species.…”

Raman Spectroscopy Technology to Monitor the Carotenoids in Skin of Thalassemia Patients: A Novel Non-Invasive Tool Relating Oxidative Stress with Iron Burden

“…28 In this work for the first time the level of dermal carotenoids, measured by Raman spectroscopy and expressed as SCS, has been assessed in patients with a transfusion-dependent thalassemia, and the use of this methodologic approach has been even in this pathology characterized by a remarkable individual oxidative stress. [1][2][3] When the SCS of thalassemia patients were correlated with hematologic parameters such as ferritin, ALT and AST, a clear inverse correlation was evident, indicating that the level of skin carotenoids can reliably be representative of the altered both iron status and hepatic pattern characterizing the pathology. As a further indication of clinical opportunity of the SCS in thalassemia, the level of skin carotenoids appeared also inversely associated with the patients' liver fibrosis, as revealed by elastography.…”

“…A characteristic depletion of antioxidant defenses and oxidative stress are associated with hematologic disorders such as b-thalassemia, [1][2][3] with the iron burden to be considered the main reason of the redox imbalance. Frequent blood transfusions and increased intestinal absorption of iron, after saturation of transferrin, indeed favor the accumulation of highly reactive low molecular weight iron in cells (labile iron pool), followed by production of various reactive oxygen species (ROS) through Fenton chemistry, oxidation of cell components, impairment of cell functions, cell death and finally organ damage.…”