scholarly journals Life and Death of Glucose-6-Phosphate Dehydrogenase (G6PD) Deficient Erythrocytes – Role of Redox Stress and Band 3 Modifications

2012 ◽  
Vol 39 (5) ◽  
pp. 328-334 ◽  
Author(s):  
Paolo Arese ◽  
Valentina Gallo ◽  
Antonella Pantaleo ◽  
Franco Turrini
Keyword(s):  
Band 3 ◽  
Redox Stress ◽  
Life And Death ◽  
Glucose 6 Phosphate Dehydrogenase

scholarly journals Band 3 Erythrocyte Membrane Protein Acts as Redox Stress Sensor Leading to Its Phosphorylation by p72Syk

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Antonella Pantaleo ◽  
Emanuela Ferru ◽  
Maria Carmina Pau ◽  
Amina Khadjavi ◽  
Giorgia Mandili ◽  
...  
Keyword(s):  
Cytoplasmic Domain ◽  
Temporal Variations ◽  
Band 3 ◽  
Serine Phosphorylation ◽  
Redox Stress ◽  
Redox Sensor ◽  
Syk Kinase ◽  
Irreversible Oxidation ◽  
Syk Inhibitor

In erythrocytes, the regulation of the redox sensitive Tyr phosphorylation of band 3 and its functions are still partially defined. A role of band 3 oxidation in regulating its own phosphorylation has been previously suggested. The current study provides evidences to support this hypothesis: (i) in intact erythrocytes, at 2 mM concentration of GSH, band 3 oxidation, and phosphorylation, Syk translocation to the membrane and Syk phosphorylation responded to the same micromolar concentrations of oxidants showing identical temporal variations; (ii) the Cys residues located in the band 3 cytoplasmic domain are 20-fold more reactive than GSH; (iii) disulfide linked band 3 cytoplasmic domain docks Syk kinase; (iv) protein Tyr phosphatases are poorly inhibited at oxidant concentrations leading to massive band 3 oxidation and phosphorylation. We also observed that hemichromes binding to band 3 determined its irreversible oxidation and phosphorylation, progressive hemolysis, and serine hyperphosphorylation of different cytoskeleton proteins. Syk inhibitor suppressed the phosphorylation of band 3 also preventing serine phosphorylation changes and hemolysis. Our data suggest that band 3 acts as redox sensor regulating its own phosphorylation and that hemichromes leading to the protracted phosphorylation of band 3 may trigger a cascade of events finally leading to hemolysis.

scholarly journals TP53-Induced Glycolysis and Apoptosis Regulator (TIGAR) Is Upregulated in Lymphocytes Stimulated with Concanavalin A

2021 ◽  
Vol 22 (14) ◽  
pp. 7436
Author(s):  
Helga Simon-Molas ◽  
Xavier Vallvé-Martínez ◽  
Irene Caldera-Quevedo ◽  
Pere Fontova ◽  
Claudia Arnedo-Pac ◽  
...  
Keyword(s):  
Concanavalin A ◽  
Carbon Flux ◽  
Human Lymphocytes ◽  
Tumor Development ◽  
Pentose Phosphate ◽  
Akt Signaling Pathway ◽  
G6pdh Activity ◽  
Physiological Conditions ◽  
Glucose 6 Phosphate Dehydrogenase

The glycolytic modulator TP53-Inducible Glycolysis and Apoptosis Regulator (TIGAR) is overexpressed in several types of cancer and has a role in metabolic rewiring during tumor development. However, little is known about the role of this enzyme in proliferative tissues under physiological conditions. In the current work, we analysed the role of TIGAR in primary human lymphocytes stimulated with the mitotic agent Concanavalin A (ConA). We found that TIGAR expression was induced in stimulated lymphocytes through the PI3K/AKT pathway, since Akti-1/2 and LY294002 inhibitors prevented the upregulation of TIGAR in response to ConA. In addition, suppression of TIGAR expression by siRNA decreased the levels of the proliferative marker PCNA and increased cellular ROS levels. In this model, TIGAR was found to support the activity of glucose 6-phosphate dehydrogenase (G6PDH), the first enzyme of the pentose phosphate pathway (PPP), since the inhibition of TIGAR reduced G6PDH activity and increased autophagy. In conclusion, we demonstrate here that TIGAR is upregulated in stimulated human lymphocytes through the PI3K/AKT signaling pathway, which contributes to the redirection of the carbon flux to the PPP.

scholarly journals Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. The role of glucose-6-phosphate dehydrogenase-derived NADPH

2009 ◽  
Vol 297 (1) ◽  
pp. H153-H162 ◽  
Author(s):  
Sabrina Serpillon ◽  
Beverly C. Floyd ◽  
Rakhee S. Gupte ◽  
Shimran George ◽  
Mark Kozicky ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Rat Heart ◽  
Mitochondrial Respiratory Chain ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Posterior Wall Thickness ◽  
Patients With Diabetes ◽  
Protein Kinase C Inhibitor ◽  
Glucose 6 Phosphate Dehydrogenase

Increased oxidative stress is a known cause of cardiac dysfunction in animals and patients with diabetes, but the sources of reactive oxygen species [e.g., superoxide anion (O2−)] and the mechanisms underlying O2− production in diabetic hearts are not clearly understood. Our aim was to determine whether NADPH oxidase (Nox) is a source of O2− and whether glucose-6-phosphate dehydrogenase (G6PD)-derived NADPH plays a role in augmenting O2− generation in diabetes. We assessed cardiac function, Nox and G6PD activities, NADPH levels, and the activities of antioxidant enzymes in heart homogenates from young (9–11 wk old) Zucker lean and obese (fa/fa) rats. We found that myocardial G6PD activity was significantly higher in fa/fa than in lean rats, whereas superoxide dismutase and glutathione peroxidase activities were decreased ( P < 0.05). O2− levels were elevated (70–90%; P < 0.05) in the diabetic heart, and this elevation was blocked by the Nox inhibitor gp-91ds-tat (50 μM) or by the mitochondrial respiratory chain inhibitors antimycin (10 μM) and rotenone (50 μM). Inhibition of G6PD by 6-aminonicotinamide (5 mM) and dihydroepiandrosterone (100 μM) also reduced ( P < 0.05) O2− production. Notably, the activities of Nox and G6PD in the fa/fa rat heart were inhibited by chelerythrine, a protein kinase C inhibitor. Although we detected no changes in stroke volume, cardiac output, or ejection fraction, left ventricular diameter was slightly increased during diastole and systole, and left ventricular posterior wall thickness was decreased during systole ( P < 0.05) in Zucker fa/fa rats. Our findings suggest that in a model of severe hyperlipidema and hyperglycemia Nox-derived O2− generation in the myocardium is fueled by elevated levels of G6PD-derived NADPH. Similar mechanisms were found to activate O2− production and induce endothelial dysfunction in aorta. Thus G6PD may be a useful therapeutic target for treating the cardiovascular disease associated with type 2 diabetes, if second-generation drugs specifically reducing the activity of G6PD to near normal levels are developed.

scholarly journals Estrogen binding by leukocytes during phagocytosis,.

1977 ◽  
Vol 145 (4) ◽  
pp. 983-998 ◽  
Author(s):  
S J Klebanoff
Keyword(s):  
Chronic Granulomatous Disease ◽  
Reaction Mechanisms ◽  
Dehydrogenase Deficiency ◽  
Cell Types ◽  
Neutrophil Function ◽  
Granulomatous Disease ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Estrogen Binding ◽  
Two Populations

Estradiol binds covalently to normal leukocytes during phagocytosis. The binding involves three cell types, neutrophils, eosinophils, and monocytes and at least two reaction mechanisms, one involving the peroxidase of neutrophils and monocytes (myeloperoxidase [MPO]) and possibly the eosinophil peroxidase, and the second involving catalase. Binding is markedly reduced when leukocytes from patients with chronic granulomatous disease (CGD), severe leukocytic glucose 6-phosphate dehydrogenase deficiency, and familial lipochrome histiocytosis are employed and two populations of neutrophils, one which binds estradiol and one which does not, can be demonstrated in the blood of a CGD carrier. Leukocytes from patients with hereditary MPO deficiency also bind estradiol poorly although the defect is not as severe as in CGD. These findings are discussed in relation to the inactivation of estrogens during infection and the possible role of estrogens in neutrophil function.

scholarly journals The role of glucose-6-phosphate dehydrogenase in adipose tissue inflammation in obesity

Adipocyte ◽  
2017 ◽  
Vol 6 (2) ◽  
pp. 147-153 ◽  
Author(s):  
Yoon Jeong Park ◽  
Sung Sik Choe ◽  
Jee Hyung Sohn ◽  
Jae Bum Kim
Keyword(s):  
Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Glucose 6 Phosphate Dehydrogenase

scholarly journals Comodulation of NO-Dependent Vasodilation by Erythroid Band 3 and Hemoglobin: A GP.Mur Athlete Study

2021 ◽  
Vol 8 ◽  
Author(s):  
Kate Hsu ◽  
Yen-Yu Liu ◽  
Wei-Chin Tseng ◽  
Kuang-Tse Huang ◽  
Chia-Yuan Liu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Occlusion ◽  
Band 3 ◽  
Flow Mediated Dilation ◽  
Red Cell Membrane ◽  
Anion Exchanger 1 ◽  
Before And After ◽  
Dependent Flow ◽  
Plasma Nitrite

GP.Mur, a red blood cell (RBC) hybrid protein encoded by glycophorin B-A-B, increases expression of erythroid band 3 (Anion Exchanger-1, SLC4A1). GP.Mur is extremely rare but has a prevalence of 1–10% in regions of Southeast Asia. We unexpectedly found slightly higher blood pressure (BP) among healthy Taiwanese adults with GP.Mur. Since band 3 has been suggested to interact with hemoglobin (Hb) to modulate nitric oxide (NO)-dependent hypoxic vasodilation during the respiratory cycle, we hypothesized that GP.Mur red cells could exert differentiable effects on vascular tone. Here we recruited GP.Mur-positive and GP.Mur-negative elite male college athletes, as well as age-matched, GP.Mur-negative non-athletes, for NO-dependent flow-mediated dilation (FMD) and NO-independent dilation (NID). The subjects were also tested for plasma nitrite and nitrate before and after arterial occlusion in FMD. GP.Mur+ and non-GP.Mur athletes exhibited similar heart rates and blood pressure, but GP.Mur+ athletes showed significantly lower FMD (4.8 ± 2.4%) than non-GP.Mur athletes (6.5 ± 2.1%). NO-independent vasodilation was not affected by GP.Mur. As Hb controls intravascular NO bioavailability, we examined the effect of Hb on limiting FMD and found it to be significantly stronger in GP.Mur+ subjects. Biochemically, plasma nitrite levels were directly proportional to individual band 3 expression on the red cell membrane. The increase of plasma nitrite triggered by arterial occlusion also showed small dependency on band 3 levels in non-GP.Mur subjects. By the GP.Mur comparative study, we unveiled comodulation of NO-dependent vasodilation by band 3 and Hb, and verified the long-pending role of erythroid band 3 in this process.

scholarly journals STUDY OF PURUSH SIDDHANT WITH SCIENTIFIC APPROACH

2021 ◽  
Vol 9 (11) ◽  
pp. 2840-2843
Author(s):  
Pramod Kumar ◽  
Pramod Kumar Prasad ◽  
Gupta S.S
Keyword(s):  
Indian Philosophy ◽  
Modern Science ◽  
Reversible Reaction ◽  
Ultimate Truth ◽  
Living World ◽  
Life And Death ◽  
Scientific Approach ◽  
The Mind ◽  
The Universe

The word “Purush" in its most social sense means man but in the aspect of Ayurveda, the term purush is repre- sented as atma or chetana dhatu (chetana-life and dhatu-element). The concept of the existence of atman (soul) is generally not accepted by modern science. According to Indian philosophy, the ultimate truth or absolute soul is one and he is Chetana (Sarvam Khalu Idam Brahm). Treatment of Panchmahabhut Sharir with presence of purush is known as Chikitsya Purush. Purush is supreme soul, pure conscious, unchanging, immortal neither birth nor death. It is essential for the creation of the universe and the living world. In the presence of purush gains knowledge through the mind. All the actions through karmendriyas, desire, pleasure, pain, life and death are per- formed. The purush (Kshetrajy) is lord of the house (Kshetra). The role of Purush in Srusti is laya & parlay which is the same as catalyst’s work in a reversible reaction. Keywords: Purush, Types, Karma Chikitsa, Chaturvinshatika, Rashi, Punarjanma

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