scholarly journals Glucose-6-phosphate dehydrogenase deficiency enhances enterovirus 71 infection

2008 ◽  
Vol 89 (9) ◽  
pp. 2080-2089 ◽  
Author(s):  
Hung-Yao Ho ◽  
Mei-Ling Cheng ◽  
Shiue-Fen Weng ◽  
Lo Chang ◽  
Tsun-Tsun Yeh ◽  
...  
Keyword(s):  
Dehydrogenase Deficiency ◽  
Enterovirus 71 ◽  
Redox Balance ◽  
Redox Status ◽  
Cellular Redox ◽  
Enteroviral Infection ◽  
Viral Progeny ◽  
Infected Cells ◽  
Exogenous Expression ◽  
Glucose 6 Phosphate Dehydrogenase

Variations in the cellular microenvironment affect the host's susceptibility to pathogens. Using glucose-6-phosphate dehydrogenase (G6PD)-deficient fibroblasts as a model, this study demonstrated that the cellular redox status affects infectivity as well as the outcome of enterovirus 71 (EV71) infection. Compared with their normal counterparts, G6PD-deficient cells supported EV71 replication more efficiently and showed greater cytopathic effect and loss of viability. Mechanistically, viral infection led to increased oxidative stress, as indicated by increased dichlorofluorescein fluorescence and a diminished ratio of glutathione (GSH) to its disulfide form (GSSG), with the effect being greater in G6PD-deficient cells. Exogenous expression of active G6PD in the deficient cells, which increased the intracellular GSH : GSSG ratio, suppressed the generation of viral progeny. Consistent with this, treatment with N-acetylcysteine offered resistance to EV71 propagation and a cytoprotective effect on the infected cells. These findings support the notion that G6PD status, and thus redox balance, is an important determinant of enteroviral infection.

scholarly journals A Regulatory Role of NAD Redox Status on Flavin Cofactor Homeostasis inS. cerevisiaeMitochondria

2013 ◽  
Vol 2013 ◽  
pp. 1-16 ◽  
Author(s):  
Teresa Anna Giancaspero ◽  
Vittoria Locato ◽  
Maria Barile
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Nicotinamide Adenine Dinucleotide ◽  
Flavin Adenine Dinucleotide ◽  
Redox Balance ◽  
Redox Status ◽  
Cellular Redox ◽  
Isolated Mitochondria ◽  
Nudix Hydrolases ◽  
Order Of Magnitude

Flavin adenine dinucleotide (FAD) and nicotinamide adenine dinucleotide (NAD) are two redox cofactors of pivotal importance for mitochondrial functionality and cellular redox balance. Despite their relevance, the mechanism by which intramitochondrial NAD(H) and FAD levels are maintained remains quite unclear inSaccharomyces cerevisiae. We investigated here the ability of isolated mitochondria to degrade externally added FAD and NAD (in both its reduced and oxidized forms). A set of kinetic experiments demonstrated that mitochondrial FAD and NAD(H) destroying enzymes are different from each other and from the already characterized NUDIX hydrolases. We studied here, in some detail, FAD pyrophosphatase (EC 3.6.1.18), which is inhibited by NAD+and NADH according to a noncompetitive inhibition, withKivalues that differ from each other by an order of magnitude. These findings, together with the ability of mitochondrial FAD pyrophosphatase to metabolize endogenous FAD, presumably deriving from mitochondrial holoflavoproteins destined to degradation, allow for proposing a novel possible role of mitochondrial NAD redox status in regulating FAD homeostasis and/or flavoprotein degradation inS. cerevisiae.

scholarly journals Redox Potential of Antioxidants in Cancer Progression and Prevention

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1156
Author(s):  
Sajan George ◽  
Heidi Abrahamse
Keyword(s):  
Oxidative Stress ◽  
Cancer Progression ◽  
Natural Antioxidants ◽  
Redox Balance ◽  
Redox Status ◽  
Enzyme Activation ◽  
Metabolic Reprogramming ◽  
Cellular Functions ◽  
Cellular Redox ◽  
The Right

The benevolent and detrimental effects of antioxidants are much debated in clinical trials and cancer research. Several antioxidant enzymes and molecules are overexpressed in oxidative stress conditions that can damage cellular proteins, lipids, and DNA. Natural antioxidants remove excess free radical intermediates by reducing hydrogen donors or quenching singlet oxygen and delaying oxidative reactions in actively growing cancer cells. These reducing agents have the potential to hinder cancer progression only when administered at the right proportions along with chemo-/radiotherapies. Antioxidants and enzymes affect signal transduction and energy metabolism pathways for the maintenance of cellular redox status. A decline in antioxidant capacity arising from genetic mutations may increase the mitochondrial flux of free radicals resulting in misfiring of cellular signalling pathways. Often, a metabolic reprogramming arising from these mutations in metabolic enzymes leads to the overproduction of so called ’oncometabolites’ in a state of ‘pseudohypoxia’. This can inactivate several of the intracellular molecules involved in epigenetic and redox regulations, thereby increasing oxidative stress giving rise to growth advantages for cancerous cells. Undeniably, these are cell-type and Reactive Oxygen Species (ROS) specific, which is manifested as changes in the enzyme activation, differences in gene expression, cellular functions as well as cell death mechanisms. Photodynamic therapy (PDT) using light-activated photosensitizing molecules that can regulate cellular redox balance in accordance with the changes in endogenous ROS production is a solution for many of these challenges in cancer therapy.

Resistance of glucose-6-phosphate dehydrogenase deficiency to malaria: effects of fava bean hydroxypyrimidine glucosides onPlasmodium falciparumgrowth in culture and on the phagocytosis of infected cells

Parasitology ◽  
1996 ◽  
Vol 113 (1) ◽  
pp. 7-18 ◽  
Author(s):  
H. Ginsburg ◽  
H. Atamna ◽  
G. Shalmiev ◽  
J. Kanaani ◽  
M. Krugliak
Keyword(s):  
Dehydrogenase Deficiency ◽  
Dietary Habits ◽  
Phagocytic Cells ◽  
Balanced Polymorphism ◽  
Fava Bean ◽  
Infected Cells ◽  
Fava Beans ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Hydrolysis Of ◽  
Selection Of

SUMMARYThe balanced polymorphism of glucose-6-phosphate dehydrogenase deficiency (G6PD-) is believed to have evolved through the selective pressure of malaria combined with consumption of fava beans. The implicated fava bean constituents are the hydroxypyrimidine glucosides vicine and convicine, which upon hydrolysis of their β-O-glucosidic bond, become potent pro-oxidants. In this work we show that the glucosides inhibit the growth ofPlasmodium falciparum, increase the hexose-monophosphate shunt activity and the phagocytosis of malaria-infected erythrocytes. These activities are exacerbated in the presence of β-glucosidase, implicating their pro-oxidant aglycones in the toxic effect, and are more pronounced in infected G6PD-erythrocytes. These results suggest that G6PD-infected erythrocytes are more susceptible to phagocytic cells, and that fava bean pro-oxidants are more efficiently suppressing parasite propagation in G6PD-erythrocytes, either by directly affecting parasite growth, or by means of enhanced phagocytic elimination of infected cells. The present findings could account for the relative resistance of G6PD-bearers to falciparum malaria, and establish a link between dietary habits and malaria in the selection of the G6PD-genotype.

scholarly journals Redox Status, Procoagulant Activity, and Metabolome of Fresh Frozen Plasma in Glucose 6-Phosphate Dehydrogenase Deficiency

2018 ◽  
Vol 5 ◽  
Author(s):  
Vassilis L. Tzounakas ◽  
Federica Gevi ◽  
Hara T. Georgatzakou ◽  
Lello Zolla ◽  
Issidora S. Papassideri ◽  
...  
Keyword(s):  
Dehydrogenase Deficiency ◽  
Redox Status ◽  
Fresh Frozen Plasma ◽  
Procoagulant Activity ◽  
Fresh Frozen ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Frozen Plasma

Glucose-6-Phosphate Dehydrogenase Deficiency in an Old Woman

2020 ◽  
Vol 6 (3) ◽  
Author(s):  
Briantais Antoine ◽  
Froidefond Margaux ◽  
Seguier Julie ◽  
Swiader Laure ◽  
Durand Jean Marc
Keyword(s):  
Dehydrogenase Deficiency ◽  
Glucose 6 Phosphate Dehydrogenase

scholarly journals Differential Expression of Peroxisomal Proteins in Distinct Types of Parotid Gland Tumors

2021 ◽  
Vol 22 (15) ◽  
pp. 7872
Author(s):  
Malin Tordis Meyer ◽  
Christoph Watermann ◽  
Thomas Dreyer ◽  
Steffen Wagner ◽  
Claus Wittekindt ◽  
...  
Keyword(s):  
Redox Balance ◽  
Matrix Proteins ◽  
Parotid Tumor ◽  
Gene Expressions ◽  
Tissue Samples ◽  
Cellular Redox ◽  
Tumor Subtypes ◽  
Parotid Tumors ◽  
Aggressive Tumors

Salivary gland cancers are rare but aggressive tumors that have poor prognosis and lack effective cure. Of those, parotid tumors constitute the majority. Functioning as metabolic machinery contributing to cellular redox balance, peroxisomes have emerged as crucial players in tumorigenesis. Studies on murine and human cells have examined the role of peroxisomes in carcinogenesis with conflicting results. These studies either examined the consequences of altered peroxisomal proliferators or compared their expression in healthy and neoplastic tissues. None, however, examined such differences exclusively in human parotid tissue or extended comparison to peroxisomal proteins and their associated gene expressions. Therefore, we examined differences in peroxisomal dynamics in parotid tumors of different morphologies. Using immunofluorescence and quantitative PCR, we compared the expression levels of key peroxisomal enzymes and proliferators in healthy and neoplastic parotid tissue samples. Three parotid tumor subtypes were examined: pleomorphic adenoma, mucoepidermoid carcinoma and acinic cell carcinoma. We observed higher expression of peroxisomal matrix proteins in neoplastic samples with exceptional down regulation of certain enzymes; however, the degree of expression varied between tumor subtypes. Our findings confirm previous experimental results on other organ tissues and suggest peroxisomes as possible therapeutic targets or markers in all or certain subtypes of parotid neoplasms.

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