Eryptosis and oxidative damage in type 2 diabetic mellitus patients with chronic kidney disease

Calderón-Salinas, José-Víctor; Muñoz-Reyes, E. G.; Guerrero-Romero, Jesús Fernando; Rodrı́guez-Morán, Martha; Bracho-Riquelme, Rodolfo Leonel; Carrera-Gracia, M. A.; Escorza, Martha Angélica Quintanar

doi:10.1007/s11010-011-0887-1

Cited by 172 publications

(145 citation statements)

References 29 publications

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“…The concentrations required for the effect are lower than those required to counteract growth of tumor cells [20]. In theory, lower garcinol concentrations may be required for triggering of eryptosis in clinical conditions associated with enhanced eryptosis susceptibility of the erythrocytes, such as dehydration [48], hyperphosphatemia [58] chronic kidney disease (CKD) [40,[61][62][63], hemolytic-uremic syndrome [64], diabetes [65], hepatic failure [66], malignancy [30], sepsis [67], Sickle-cell disease [30], beta-thalassemia [30], Hb-C and G6PD-deficiency [30], as well as Wilsons disease [68]. In those disorders lower garcinol concentrations may be sufficient to trigger eryptosis.…”

Section: Discussionmentioning

confidence: 99%

Stimulation of Suicidal Erythrocyte Death by Garcinol

Fazio

Briglia

Faggio

et al. 2015

Cell Physiol Biochem

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Background/Aims: The benzophenone garcinol from dried fruit rind of Garcinia indica counteracts malignancy, an effect at least in part due to stimulation of apoptosis. The proapototic effect of garcinol is attributed in part to inhibition of histone acetyltransferases and thus modification of gene expression. Moreover, garcinol triggers mitochondrial depolarisation. Erythrocytes lack gene expression and mitochondria but are nevertheless able to enter apoptosis-like suicidal death or eryptosis, which is characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Stimulators of eryptosis include oxidative stress, energy depletion and Ca 2+ entry with increase of cytosolic Ca 2+ activity ([Ca 2+ ] i ). The present study explored, whether and how garcinol induces eryptosis. Methods: To this end, phosphatidylserine exposure at the cell surface was estimated from annexin-V-binding, cell volume from forward scatter, hemolysis from hemoglobin release, [Ca 2+ ] i from Fluo3-fluorescence, ROS formation from DCFDA dependent fluorescence and cytosolic ATP levels utilizing a luciferin-luciferase-based assay. Results: A 24 hours exposure of human erythrocytes to garcinol (2.5 or 5 µM) significantly increased the percentage of annexin-V-binding cells. Garcinol decreased (at 1 µM and 2.5 µM) or increased (at 5 µM) forward scatter. Garcinol (5 µM) further increased Fluo3-fluorescence, increased DCFDA fluorescence, and decreased cytosolic ATP levels. The effect of garcinol on annexin-V-binding was significantly blunted, but not abolished by removal of extracellular Ca 2+ . Conclusions: Garcinol triggers cell shrinkage and phospholipid scrambling of the erythrocyte cell membrane, an effect in part due to stimulation of ROS formation, energy depletion and Ca 2+ entry.

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Section: Discussionmentioning

confidence: 99%

Stimulation of Suicidal Erythrocyte Death by Garcinol

Fazio

Briglia

Faggio

et al. 2015

Cell Physiol Biochem

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“…In vitro and in vivo assays in which erythrocyte metabolic alterations were associated to oxidant environments induced increased lipoperoxidation (Quintanar-Escorza et al, 2010;Calderón-Salinas et al, 2011).…”

Section: Protein Modificationsmentioning

confidence: 99%

“…Under this condition, free www.intechopen.com Anemia 30 radical formation may play a role in the pathophysiology of several diseases. There is evidence that erythrocytes undergo oxidative changes in conditions where free radical formation is known to be high such as rheumatoid arthritis (Richards et al, 2007), diabetes (Manuel y Keenoy et al, 2001;Calderón-Salinas et al, 2011), and hemodialysis treatment (Zachee et al, 1988). Oxidative damage was also considered the cause of decreased deformability and altered rheology of erythrocytes found in individuals with chronic fatigue syndrome, a condition that may be triggered by certain infectious diseases, multiple nutrient deficiencies, food intolerance, or extreme physical or mental stress (Richards et al, 2007).…”

Section: In Vivo Erythrocyte Death and Possible Preventionmentioning

confidence: 99%

Erythrocyte: Programmed Cell Death

Vittori¹,

Vota²,

Nesse³

2012

Anemia

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“…Eryptosis is triggered by a wide variety of xenobiotics [46,. Eryptosis is further enhanced by a variety of clinical conditions, including dehydration [63], hyperphosphatemia [73], chronic kidney disease (CKD) [55,[76][77][78], haemolytic uraemic syndrome [79], diabetes [80], hepatic failure [81], malignancy [46], sepsis [82], sickle-cell disease [46], beta-thalassaemia [46], Hb-C deficiency [46], G6PD deficiency [46] and Wilson's disease [83]. This study explored whether nigericin is capable of triggering eryptosis.…”

mentioning

confidence: 99%

Triggering of Suicidal Erythrocyte Death by the Antibiotic Ionophore Nigericin

Bissinger

Malik

Bouguerra

et al. 2015

Basic Clin Pharma Tox

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The K + ,H + ionophore and antibiotic nigericin has been shown to trigger apoptosis and is thus considered for the treatment of malignancy. Cellular mechanisms involved include induction of oxidative stress, which is known to activate erythrocytic Ca 2+ -permeable unselective cation channels leading to Ca 2+ entry, increase in cytosolic Ca 2+ activity ([Ca 2+ ] i ) and subsequent stimulation of eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. This study explored whether and how nigericin induces eryptosis. Phosphatidylserine exposure at the cell surface was estimated from annexin V binding, cell volume from forward scatter, [Ca 2+ ] i from Fluo3 fluorescence, pH i from BCECF fluorescence, ceramide abundance utilizing antibodies and reactive oxygen species (ROS) formation from DCFDA-dependent fluorescence. A 48-hr exposure of human erythrocytes to nigericin significantly increased the percentage of annexin-V-binding cells (0.1-10 nM), significantly decreased forward scatter (0.1-1 nM), significantly decreased cytosolic pH (0.1-1 nM) and significantly increased Fluo3 fluorescence (0.1-10 nM). Nigericin (1 nM) slightly, but significantly, increased ROS, but did not significantly modify ceramide abundance. Materials and MethodsErythrocytes, solutions and chemicals. Li-heparin-anticoagulated fresh blood samples were kindly provided by the blood bank of the University of T€ ubingen. The study was approved by the ethics committee of the University of T€ ubingen (184/2003 V). The blood was centrifuged at 120 9 g for 20 min. at 21°C and the platelet-and leucocyte-containing supernatant were disposed. Erythrocytes were incubated in vitro at a haematocrit of 0.4% in Ringer solution containing (in mM) 125 NaCl, 5 KCl, 1 MgSO 4 , 32 N-2-hydroxyethylpiperazine-N-2-ethanesulfonic acid (HEPES; pH 7.4), 5 glucose and 1 CaCl 2 , at 37°C for 48 hr. Where indicated, erythrocytes were exposed to nigericin (Enzo Life Sciences, L€ orrach, Germany) at the indicated concentrations.Annexin V binding and forward scatter. After incubation under the respective experimental condition, a 150-ll cell suspension was centrifuged at 350 rcf for 3 min. and, after trashing the supernatant,

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Eryptosis and oxidative damage in type 2 diabetic mellitus patients with chronic kidney disease

Cited by 172 publications

References 29 publications

Stimulation of Suicidal Erythrocyte Death by Garcinol

Stimulation of Suicidal Erythrocyte Death by Garcinol

Erythrocyte: Programmed Cell Death

Triggering of Suicidal Erythrocyte Death by the Antibiotic Ionophore Nigericin

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