Abstract
Reactive oxygen species (ROS) released in cells are signaling molecules but can also modify signaling proteins. Red blood cells perform a major role in maintaining the balance of the redox in the blood. The main cytosolic protein of RBC is hemoglobin (Hb), which accounts for 95-97%. Most other proteins are involved in protecting the blood cell from oxidative stress. Hemoglobin is a major factor in initiating oxidative stress within the erythrocyte. RBCs can also be damaged by exogenous oxidants. Hb autoxidation leads to the generation of a superoxide radical, of which the catalyzed or spontaneous dismutation produces hydrogen peroxide. Both oxidants induce hemichrome formation, heme degradation, and release of free iron which is a catalyst for free radical reactions. To maintain the redox balance, appropriate antioxidants are present in the cytosol, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and peroxiredoxin 2 (PRDX2), as well as low molecular weight antioxidants: glutathione, ascorbic acid, lipoic acid, α-tocopherol, β-carotene, and others. Redox imbalance leads to oxidative stress and may be associated with overproduction of ROS and/or insufficient capacity of the antioxidant system. Oxidative stress performs a key role in CKD as evidenced by the high level of markers associated with oxidative damage to proteins, lipids, and DNA in vivo. In addition to the overproduction of ROS, a reduced antioxidant capacity is observed, associated with a decrease in the activity of SOD, GPx, PRDX2, and low molecular weight antioxidants. In addition, hemodialysis is accompanied by oxidative stress in which low-biocompatibility dialysis membranes activate phagocytic cells, especially neutrophils and monocytes, leading to a respiratory burst. This review shows the production of ROS under normal conditions and CKD and its impact on disease progression. Oxidative damage to red blood cells (RBCs) in CKD and their contribution to cardiovascular disease are also discussed.
Highlights
Chronic kidney disease (CKD) is a pathological condition in which, as a result of impaired excretory function, associated with a decrease in the number of nephrons, toxic substances accumulate in the body
Their increased production and/or insufficient performance of antioxidant systems can lead to oxidative stress which is associated with the damage or/and oxidative modification of vital molecules such as nucleic acid, proteins, and lipids [2]
We showed that red blood cells (RBCs) from CKD patients were significantly more sensitive to oxidative stress induced by hydrogen peroxide than erythrocytes from healthy subjects [146]
Summary
Chronic kidney disease (CKD) is a pathological condition in which, as a result of impaired excretory function, associated with a decrease in the number of nephrons, toxic substances accumulate in the body. The release of ROS in the body is related to their physiological role as signaling molecules Their increased production and/or insufficient performance of antioxidant systems can lead to oxidative stress which is associated with the damage or/and oxidative modification of vital molecules such as nucleic acid, proteins (enzymes), and lipids [2]. Oxidative stress performs a key role in disease progression as evidenced by the high level of markers associated with oxidative damage to proteins, lipids, and DNA in vivo. The oxidative damage of red blood cells in CKD, which affects the rheological properties of the blood but is associated with the development of cardiovascular diseases, was taken into consideration. We emphasize the role of oxidative stress, which disrupts redox homeostasis, exacerbates the disease in patients with chronic kidney disease, and is a major contributor to the cardiovascular disease that accompanies chronic kidney disease
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