China
Africa
Explore chapters and articles related to this topic
Dopamine in the Immune and Hematopoietic Systems
Published in Nira Ben-Jonathan, Dopamine, 2020
A well-studied function of DA in erythrocytes is inhibition of apoptosis, which is normally triggered by oxidative stress, hypertonic shock, removal of extracellular Cl−, or energy depletion. To distinguish between apoptosis of nucleated cells and that in erythrocytes, the term “eryptosis” was coined [27]. In this study, treatment of erythrocytes with ionomycin, a Ca2+ ionophore, led to cell shrinkage, cell membrane blebbing and breakdown of membrane phosphatidylserine asymmetry, all typical features of apoptosis in nucleated cells. Several catecholamines, including DA, inhibited the activated entry of Ca2+ into erythrocytes by removal of Cl−, thus preventing the increase of cytosolic Ca2+ activity that causes cell shrinkage. The authors concluded that the effect of catecholamines on apoptosis is due to a direct or an indirect inactivation of the calcium-permeable, nonselective cation conductance.
Hyperglycemia Impairs the Functions of Blood
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
However, hemolysis, eryptosis, calcium accumulation, loss of glutathione, and increase in the ratio of GSSG/GSH (oxidized to reduced glutathione) were attenuated by high glucose, apparently due to maintenance of energy supply to the cells. Loss of plasma membrane Ca2+-ATPase activity and decrease in superoxide production were not affected by glucose concentration, being seemingly determined by processes independent of both glycoxidation and energy depletion.
Artemether–Lumefantrine
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Robert J. Commons, Julie A. Simpson, Ric N. Price
The physicochemical and structural similarities of lumefantrine to other arylamino class II blood schizontocidal anti-malarial compounds (e.g. mefloquine and halofantrine) suggest a common mode of action for these drugs. Although the mechanism of action is not completely understood, it is thought that they achieve their anti-malarial activity in the parasite’s acid food vacuole or cytoplasm (Combrinck et al., 2013). During parasite development, hemoglobin is broken down to form ferriprotoporphyrin IX (heme). Free heme is toxic to the parasite but is detoxified by being complexed into malarial pigment (hemozoin). Both quinine and chloroquine bind to the heme monomer, preventing polymerization and thus iron detoxification. A similar anti-parasitic activity is also proposed for lumefantrine (Combrinck et al., 2013). Lumefantrine may also cause eryptosis, or suicidal death of infected erythrocytes, in which cell surface changes result in early removal from the circulating blood and a subsequent reduction in parasitemia (Alzoubi et al., 2014).
Assessing regulated cell death modalities as an efficient tool for in vitro nanotoxicity screening: a review
Published in Nanotoxicology, 2023
Anton Tkachenko, Anatolii Onishchenko, Valeriy Myasoedov, Svetlana Yefimova, Ondrej Havranek
Eryptosis is a regulated cell death mode of non-nucleated cells, such as erythrocytes (Pretorius, Du Plooy, and Bester 2016; Repsold and Joubert 2018). Eryptosis morphologically resembles apoptosis of nucleated cells. It is associated with cell shrinkage, phosphatidylserine externalization, and membrane blebbing (microvesiculation of cell membranes). In contrast to hemolysis, the cell membrane remains intact (Lang et al. 2006). Influx of Ca2+ is considered as a critical event in eryptosis that leads to the opening of Ca2+-dependent K+-channels referred to as Gardos channels to promote cell shrinkage. The Ca2+ influx is accompanied by ROS overgeneration, sphingomyelinase-dependent ceramide generation by sphingomyelin hydrolysis, and calpain activation (Dreischer et al. 2022). Eryptosis could be triggered, e.g. by oxidative stress, hyperosmolar conditions, energy insufficiency, or xenobiotics (Lang and Lang 2015; Tkachenko et al. 2021; Tkachenko and Onishchenko 2023). Importantly, an increasing number of evidences suggest that eryptosis is accelerated and might contribute to the pathophysiology of various diseases including anemia, chronic inflammation, diabetes mellitus, arterial hypertension, sepsis, or hepatic and renal disorders (Qadri et al. 2017; Bissinger et al. 2019; Restivo et al. 2021).
Metformin protects red blood cells against rotenone induced oxidative stress and cytotoxicity
Published in Archives of Physiology and Biochemistry, 2021
Shambhoo Sharan Tripathi, Abhishek Kumar Singh, Farhan Akhtar, Ankita Chaudhary, Syed Ibrahim Rizvi
The present investigation was undertaken to evaluate the anti-oxidative potential of metformin to limit rotenone-induced toxicity in blood. Rotenone is a widely used plant-derived broad-spectrum pesticide (piscicide, acaricide, and insecticide). Being extremely hydrophobic, rotenone can easily cross biological membranes, apparently without a transport system (Esteve-Rudd et al.2011). According to WHO classification, rotenone is a dangerous Class II pesticide. Rotenone induces toxicity through ROS over-production and oxidative stress (Sherer et al.2003), which further leads to a neurodegenerative disorder like Parkinson’s disease (PD) (Tanner et al.2011). It has also been observed that rotenone induces eryptosis, a common cell death mechanism of erythrocytes. In addition, it induces cell membrane scrambling that results in erythrocytes shrinkage (Lupescu et al.2012). As a consequence, rotenone toxicity may lead to premature removal of circulating erythrocytes (Jelkmann 2012). The disproportionate eryptosis may also lead to anaemia (Lang et al.2008), significantly a higher incidence of anaemia has been reported in patients with PD (Kasten et al.2010). The anaemia could also be an early symptom for other neurological disorders (Kasten et al.2010, Savica et al.2010).
Beyond neurodegenerative diseases: α-synuclein in erythropoiesis
Published in Hematology, 2022
Ling Ling, Fangfang Wang, Duonan Yu
The presence of anemia or low hemoglobin levels are often associated with PD [51,60]. A recent study demonstrated that patients with newly diagnosed anemia have higher risk developing PD after four years [61]. By observing the ultrastructure of erythrocytes in patients with PD, the shape of erythrocytes is found to be changed, including phospholipid membrane scrambling, membrane blebbing and cell shrinkage, all of which are the characteristics of eryptosis, a class of programed cell death [62].