Abstract
Erythrocytes play an important role in oxygen and carbon dioxide transport. Although erythrocytes possess no nucleus or mitochondria, they fulfil several metabolic activities namely, the Embden-Meyerhof pathway, as well as the hexose monophosphate shunt. Metabolic processes within the erythrocyte contribute to the morphology/shape of the cell and important constituents are being kept in an active, reduced form. Erythrocytes undergo a form of suicidal cell death called eryptosis. Eryptosis results from a wide variety of contributors including hyperosmolarity, oxidative stress, and exposure to xenobiotics. Eryptosis occurs before the erythrocyte has had a chance to be naturally removed from the circulation after its 120-day lifespan and is characterised by the presence of membrane blebbing, cell shrinkage, and phosphatidylserine exposure that correspond to nucleated cell apoptotic characteristics. After eryptosis is triggered there is an increase in cytosolic calcium (Ca2+) ion levels. This increase causes activation of Ca2+-sensitive potassium (K+) channels which leads to a decrease in intracellular potassium chloride (KCl) and shrinkage of the erythrocyte. Ceramide, produced by sphingomyelinase from the cell membrane's sphingomyelin, contributes to the occurrence of eryptosis. Eryptosis ensures healthy erythrocyte quantity in circulation whereas excessive eryptosis may set an environment for the clinical presence of pathophysiological conditions including anaemia.
Highlights
Erythrocytes are derived from haematopoietic stem cells in the red bone marrow by the production of a cytokine erythropoietin produced in the kidneys [1]
Mature erythrocytes still possess erythropoietin receptors which influence the prevalence of eryptosis in erythrocytes through regulation of the cation channels [95]
Even though erythrocytes are constantly exposed to extreme conditions, they manage to repair some of the damage without the presence of a nucleus or mitochondria
Summary
Erythrocytes are derived from haematopoietic stem cells in the red bone marrow by the production of a cytokine erythropoietin produced in the kidneys [1]. Cell shrinkage in eryptosis results from activation of Ca2+-sensitive K+ channels leading to a loss of KCl from the erythrocyte ensued by the loss of water [9]. Ceramide is common in the presence of osmotic shock since it stimulates release of PAF by the activation of phospholipase and, as a result of the ceramide on the cell membrane, PAF produces a scrambled sarcolemma that leads to exposure of phosphatidylserine on the erythrocyte membrane. This effect of ceramide may result from the fact that ceramide induces transbilayer lipid movement [2]. The process of eryptosis regulation is especially complex, implicating a multitude of cellular machinery and various triggers, inhibitors, and diseases in its mechanism of action [16, 17]
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