Suicidal Erythrocyte Death in Metabolic Syndrome

Restivo, Ignazio; Attanzio, Alessandro; Tesoriere, Luisa; Allegra, Mario

doi:10.3390/antiox10020154

Cited by 19 publications

(24 citation statements)

References 102 publications

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“…In this context, eryptosis has been reported to occur [110]. In fact, in the metabolic syndrome which represents a disorder that combines hyperglycemia, dyslipidemia, hypertension, and obesity and leads to diabetes and atherosclerosis, increased eryptosis is already observed [111]. In vivo, an acute hyperglycemic "spike", which is a situation associated with a rise in oxidant stress in diabetes, has been shown to impair blood rheology [112].…”

Section: Rbcs and Their Energy Needsmentioning

confidence: 99%

Metabolic Influences Modulating Erythrocyte Deformability and Eryptosis

et al. 2021

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Many factors in the surrounding environment have been reported to influence erythrocyte deformability. It is likely that some influences represent reversible changes in erythrocyte rigidity that may be involved in physiological regulation, while others represent the early stages of eryptosis, i.e., the red cell self-programmed death. For example, erythrocyte rigidification during exercise is probably a reversible physiological mechanism, while the alterations of red blood cells (RBCs) observed in pathological conditions (inflammation, type 2 diabetes, and sickle-cell disease) are more likely to lead to eryptosis. The splenic clearance of rigid erythrocytes is the major regulator of RBC deformability. The physicochemical characteristics of the surrounding environment (thermal injury, pH, osmolality, oxidative stress, and plasma protein profile) also play a major role. However, there are many other factors that influence RBC deformability and eryptosis. In this comprehensive review, we discuss the various elements and circulating molecules that might influence RBCs and modify their deformability: purinergic signaling, gasotransmitters such as nitric oxide (NO), divalent cations (magnesium, zinc, and Fe++), lactate, ketone bodies, blood lipids, and several circulating hormones. Meal composition (caloric and carbohydrate intake) also modifies RBC deformability. Therefore, RBC deformability appears to be under the influence of many factors. This suggests that several homeostatic regulatory loops adapt the red cell rigidity to the physiological conditions in order to cope with the need for oxygen or fuel delivery to tissues. Furthermore, many conditions appear to irreversibly damage red cells, resulting in their destruction and removal from the blood. These two categories of modifications to erythrocyte deformability should thus be differentiated.

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Section: Rbcs and Their Energy Needsmentioning

confidence: 99%

Metabolic Influences Modulating Erythrocyte Deformability and Eryptosis

et al. 2021

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“…The major trigger of eryptosis is the increase of cytosolic Ca 2+ activity resulting from Ca 2+ entry through Ca 2+ -permeable unselective cation channels (permeable to both Na + and Ca 2+ ) [ 60 ]. Instead, Ca 2+ entry and Ca 2+ -dependent RBCs membrane scrambling do not require caspases activation [ 61 , 62 ].…”

Section: Introductionmentioning

confidence: 99%

Usnic Acid and Usnea barbata (L.) F.H. Wigg. Dry Extracts Promote Apoptosis and DNA Damage in Human Blood Cells through Enhancing ROS Levels

et al. 2021

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Nowadays, numerous biomedical studies performed on natural compounds and plant extracts aim to obtain highly selective pharmacological activities without unwanted toxic effects. In the big world of medicinal plants, Usnea barbata (L) F.H. Wigg (U. barbata) and usnic acid (UA) are well-known for their therapeutical properties. One of the most studied properties is their cytotoxicity on various tumor cells. This work aims to evaluate their cytotoxic potential on normal blood cells. Three dry U. barbata extracts in various solvents: ethyl acetate (UBEA), acetone (UBA), and ethanol (UBE) were prepared. From UBEA we isolated usnic acid with high purity by semipreparative chromatography. Then, UA, UBA, and UBE dissolved in 1% dimethyl sulfoxide (DMSO) and diluted in four concentrations were tested for their toxicity on human blood cells. The blood samples were collected from a healthy non-smoker donor; the obtained blood cell cultures were treated with the tested samples. After 24 h, the cytotoxic effect was analyzed through the mechanisms that can cause cell death: early and late apoptosis, caspase 3/7 activity, nuclear apoptosis, autophagy, reactive oxygen species (ROS) level and DNA damage. Generally, the cytotoxic effect was directly proportional to the increase of concentrations, usnic acid inducing the most significant response. At high concentrations, usnic acid and U. barbata extracts induced apoptosis and DNA damage in human blood cells, increasing ROS levels. Our study reveals the importance of prior natural products toxicity evaluation on normal cells to anticipate their limits and benefits as potential anticancer drugs.

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“…Under physiological conditions, Ca 2+ homeostasis is regulated through the complementary actions of both Ca 2+ pumps, that act through ATP-dependent extrusion mechanisms, and Ca 2+ channels, that allow extracellular Ca 2+ to enters [6]. Pro-eryptotic stimuli activate phospholipase A2 (PLA2) that releases arachidonic acid (AA) (1).…”

Section: Mechanisms Of the Eryptotic Machinerymentioning

confidence: 99%

Anti-Eryptotic Activity of Food-Derived Phytochemicals and Natural Compounds

Restivo

Attanzio

Tesoriere

et al. 2022

IJMS

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Human red blood cells (RBCs), senescent or damaged due to particular stress, can be removed by programmed suicidal death, a process called eryptosis. There are various molecular mechanisms underlying eryptosis. The most frequent is the increase in the cytoplasmic concentration of Ca2+ ions, later exposure of erythrocytes to oxidative stress, hyperosmotic shock, ceramide formation, stimulation of caspases, and energy depletion. Phosphatidylserine (PS) exposed by eryptotic RBCs due to interaction with endothelial CXC-Motiv-Chemokin-16/Scavenger-receptor, causes the RBCs to adhere to vascular wall with consequent damage to the microcirculation. Eryptosis can be triggered by various xenobiotics and endogenous molecules, such as high cholesterol levels. The possible diseases associated with eryptosis are various, including anemia, chronic kidney disease, liver failure, diabetes, hypertension, heart failure, thrombosis, obesity, metabolic syndrome, arthritis, and lupus. This review addresses and collates the existing ex vivo and animal studies on the inhibition of eryptosis by food-derived phytochemicals and natural compounds including phenolic compounds (PC), alkaloids, and other substances that could be a therapeutic and/or co-adjuvant option in eryptotic-driven disorders, especially if they are introduced through the diet.

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Suicidal Erythrocyte Death in Metabolic Syndrome

Cited by 19 publications

References 102 publications

Metabolic Influences Modulating Erythrocyte Deformability and Eryptosis

Metabolic Influences Modulating Erythrocyte Deformability and Eryptosis

Usnic Acid and Usnea barbata (L.) F.H. Wigg. Dry Extracts Promote Apoptosis and DNA Damage in Human Blood Cells through Enhancing ROS Levels

Anti-Eryptotic Activity of Food-Derived Phytochemicals and Natural Compounds

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