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G6PD oxidative stress

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https://www.readbyqxmd.com/read/28208930/precautionary-measures-for-successful-open-heart-surgery-in-g6pd-deficient-patient-a-case-report
#1
Rupesh Kumar
Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is among the most common enzymatic disorders of red blood cells. Cardiac surgeries on this group of individuals are associated with an additional risk in terms of impaired oxygenation, prolonged ventilation and increased risk of haemolysis. These patients have a very low threshold for haemolysis due to oxidative stress. Many commonly used drugs also predispose the individual for haemolysis when they are subjected to surgery. Here we present a known case of G6PD deficient patient with symptoms of breathlessness for the last nine years who was taken for surgery with pre-planned precautionary measures to avoid unnecessary haemolysis...
December 2016: Journal of Clinical and Diagnostic Research: JCDR
https://www.readbyqxmd.com/read/28185390/oxidative-stress-as-a-damage-mechanism-in-porcine-cumulus-oocyte-complexes-exposed-to-malathion-during-in-vitro-maturation
#2
Diana Flores, Verónica Souza, Miguel Betancourt, Mario Teteltitla, Humberto González-Márquez, Eduardo Casas, Edmundo Bonilla, Patricia Ramírez-Noguera, María Concepción Gutiérrez-Ruíz, Yvonne Ducolomb
Malathion is one of the most commonly used insecticides. Recent findings have demonstrated that it induces oxidative stress in somatic cells, but there are not enough studies that have demonstrated this effect in germ cells. Malathion impairs porcine oocyte viability and maturation, but studies have not shown how oxidative stress damages maturation and which biochemical mechanisms are affected in this process in cumulus-oocyte complexes (COCs). The aims of the present study were to determine the amount of oxidative stress produced by malathion in porcine COCs matured in vitro, to define how biochemical mechanisms affect this process, and determine whether trolox can attenuate oxidative damage...
February 10, 2017: Environmental Toxicology
https://www.readbyqxmd.com/read/28103909/potential-diagnostic-biomarkers-for-chronic-kidney-disease-of-unknown-etiology-ckdu-in-sri-lanka-a-pilot-study
#3
Saravanabavan Sayanthooran, Dhammika N Magana-Arachchi, Lishanthe Gunerathne, Tilak Abeysekera
BACKGROUND: In Sri Lanka, there exists chronic kidney disease of both known (CKD) and unknown etiologies (CKDu). Identification of novel biomarkers that are customized to the specific causative factors would lead to early diagnosis and clearer prognosis of the diseases. This study aimed to find genetic biomarkers in blood to distinguish and identify CKDu from CKD as well as healthy populations from CKDu endemic and non-endemic areas of Sri Lanka. METHODS: The expression patterns of a selected panel of 12 potential genetic biomarkers were analyzed in blood using RT-qPCR...
January 19, 2017: BMC Nephrology
https://www.readbyqxmd.com/read/28096627/altered-oxidative-stress-and-carbohydrate-metabolism-in-canine-mammary-tumors
#4
K Jayasri, K Padmaja, M Saibaba
AIM: Mammary tumors are the most prevalent type of neoplasms in canines. Even though cancer induced metabolic alterations are well established, the clinical data describing the metabolic profiles of animal tumors is not available. Hence, our present investigation was carried out with the aim of studying changes in carbohydrate metabolism along with the level of oxidative stress in canine mammary tumors. MATERIALS AND METHODS: Fresh mammary tumor tissues along with the adjacent healthy tissues were collected from the college surgical ward...
December 2016: Veterinary World
https://www.readbyqxmd.com/read/28090457/glucose-6-phosphate-dehydrogenase-deficiency-does-not-increase-the-susceptibility-of-sperm-to-oxidative-stress-induced-by-h2o2
#5
Shiva Roshankhah, Zahra Rostami-Far, Farhad Shaveisi-Zadeh, Abolfazl Movafagh, Mitra Bakhtiari, Jila Shaveisi-Zadeh
OBJECTIVE: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzyme defect. G6PD plays a key role in the pentose phosphate pathway, which is a major source of nicotinamide adenine dinucleotide phosphate (NADPH). NADPH provides the reducing equivalents for oxidation-reduction reductions involved in protecting against the toxicity of reactive oxygen species such as H2O2. We hypothesized that G6PD deficiency may reduce the amount of NADPH in sperms, thereby inhibiting the detoxification of H2O2, which could potentially affect their motility and viability, resulting in an increased susceptibility to infertility...
December 2016: Clinical and Experimental Reproductive Medicine
https://www.readbyqxmd.com/read/28079896/impaired-embryonic-development-in-glucose-6-phosphate-dehydrogenase-deficient-caenorhabditis-elegans-due-to-abnormal-redox-homeostasis-induced-activation-of-calcium-independent-phospholipase-and-alteration-of-glycerophospholipid-metabolism
#6
Tzu-Ling Chen, Hung-Chi Yang, Cheng-Yu Hung, Meng-Hsin Ou, Yi-Yun Pan, Mei-Ling Cheng, Arnold Stern, Szecheng J Lo, Daniel Tsun-Yee Chiu
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a commonly pervasive inherited disease in many parts of the world. The complete lack of G6PD activity in a mouse model causes embryonic lethality. The G6PD-deficient Caenorhabditis elegans model also shows embryonic death as indicated by a severe hatching defect. Although increased oxidative stress has been implicated in both cases as the underlying cause, the exact mechanism has not been clearly delineated. In this study with C. elegans, membrane-associated defects, including enhanced permeability, defective polarity and cytokinesis, were found in G6PD-deficient embryos...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28041936/the-regulation-of-the-pentose-phosphate-pathway-remember-krebs
#7
REVIEW
Juan Ignacio Ramos-Martinez
The changes in gene expression and posttranslational modifications of enzymes are comprised in the concept of "coarse control" of the oxidative phase of the pentose phosphate pathway. However, these changes are slow in its implementation. The defensive mechanism against oxidative stress requires a most rapid response, impossible to achieve with coarse regulation systems. Recently, it has been suggested that a quick acceleration mechanism of G6PD activity could be produced by the reduction of NADPH-inhibition of G6PD...
January 15, 2017: Archives of Biochemistry and Biophysics
https://www.readbyqxmd.com/read/27981932/g6pd-deficiency-with-arnold-chiari-malformation
#8
Shilpi Verma, Pradeep Kumar Bhatia, Vandana Sharma, Priyanka Sethi, Yogendra Raj Singh
A neonate with glucose-6-phosphate dehydrogenase (G6PD) deficiency and Arnold-Chiari Malformation (ACM) type 2 underwent lumbar meningomyelocele (MMC) repair. Patients with G6PD deficiency are prone to develop haemolysis following any kind of oxidative stress and in ACM, there is a disturbed cranio-spinal pressure relationship. The neonate was managed under general anaesthesia with propofol for induction as well as for maintenance along with fentanyl and oxygen-nitrous mixture.
November 2016: Journal of the College of Physicians and Surgeons—Pakistan: JCPSP
https://www.readbyqxmd.com/read/27975059/upregulation-of-oxidative-stress-related-genes-in-a-chronic-kidney-disease-attributed-to-specific-geographical-locations-of-sri-lanka
#9
Saravanabavan Sayanthooran, Dhammika N Magana-Arachchi, Lishanthe Gunerathne, Tilak D J Abeysekera, Suneth S Sooriyapathirana
Objective. To infer the influence of internal and external oxidative stress in chronic kidney disease patients of unknown etiology (CKDu) in Sri Lanka, by analyzing expression of genes related directly or indirectly to oxidative stress: glutamate-cysteine ligase catalytic subunit (GCLC), glutathione S-transferase mu 1 (GSTM1), glucose-6-phosphate dehydrogenase (G6PD), fibroblast growth factor-23 (FGF23), and NLR family pyrin domain containing 3 (NLRP3). Methods. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was carried out for the selected populations: CKDu patients (n = 43), chronic kidney disease patients (CKD; n = 14), healthy individuals from a CKDu endemic area (GHI; n = 9), and nonendemic area (KHI; n = 16)...
2016: BioMed Research International
https://www.readbyqxmd.com/read/27888691/redox-imbalance-and-mitochondrial-abnormalities-in-the-diabetic-lung
#10
Jinzi Wu, Zhen Jin, Liang-Jun Yan
Although the lung is one of the least studied organs in diabetes, increasing evidence indicates that it is an inevitable target of diabetic complications. Nevertheless, the underlying biochemical mechanisms of lung injury in diabetes remain largely unexplored. Given that redox imbalance, oxidative stress, and mitochondrial dysfunction have been implicated in diabetic tissue injury, we set out to investigate mechanisms of lung injury in diabetes. The objective of this study was to evaluate NADH/NAD(+) redox status, oxidative stress, and mitochondrial abnormalities in the diabetic lung...
November 17, 2016: Redox Biology
https://www.readbyqxmd.com/read/27880809/molecular-analysis-of-glucose-6-phosphate-dehydrogenase-gene-mutations-in-bangladeshi-individuals
#11
Suprovath Kumar Sarker, Md Tarikul Islam, Grace Eckhoff, Mohammad Amir Hossain, Syeda Kashfi Qadri, A K M Muraduzzaman, Golam Sarower Bhuyan, Mohammod Shahidullah, Mohammad Abdul Mannan, Sarabon Tahura, Manzoor Hussain, Shahida Akhter, Nazmun Nahar, Tahmina Shirin, Firdausi Qadri, Kaiissar Mannoor
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common X-linked human enzyme defect of red blood cells (RBCs). Individuals with this gene defect appear normal until exposed to oxidative stress which induces hemolysis. Consumption of certain foods such as fava beans, legumes; infection with bacteria or virus; and use of certain drugs such as primaquine, sulfa drugs etc. may result in lysis of RBCs in G6PD deficient individuals. The genetic defect that causes G6PD deficiency has been identified mostly as single base missense mutations...
2016: PloS One
https://www.readbyqxmd.com/read/27872579/simultaneous-dual-targeting-of-par-4-and-g6pd-a-promising-new-approach-in-cancer-therapy-quintessence-of-a-literature-review-on-survival-requirements-of-tumor-cells
#12
Ingeborg Elisabeth Cernaj
: The aim of this hypothesis is to propose a new approach in targeted therapy of cancer: The simultaneous, dual targeting of two single molecules, Par-4 and G6PD, rather than inhibition of full-length signaling pathways. RATIONALE: Targeted inhibition of especially two survival signaling pathways (PI3K/AKT/mTOR and MAPK/ERK) is frequently tried, however, a major breakthrough has not yet been reported. Inhibition of complete pathways naturally goes along with a variety of dose-limiting side effects thus contributing to poor efficacy of the administered drugs...
2016: Cancer Cell International
https://www.readbyqxmd.com/read/27868087/diabetic-wound-healing-and-activation-of-nrf2-by-herbal-medicine
#13
Donald R Senger, Shugeng Cao
Nrf2 defense is a very important cellular mechanism to control oxidative stress, which is implicated in wound healing. Nrf2 can induce many cytoprotective genes, including HO-1, NQO1 and G6PD. Among many natural products that have been reported as Nrf2 activators, sulforaphane and curcumin have been studied more widely than any others, and both are in clinical trials for non-cancerous disorders. Recently, we reported 4-ethyl catechol and 4-vinyl catechol as Nrf2 co-factors that can induce Nrf2 as potently as sulforaphane and curcumin...
2016: Journal of Nature and Science
https://www.readbyqxmd.com/read/27855617/eryptosis-ally-or-enemy
#14
Marilena Briglia, Maria Antonia Rossi, Caterina Faggio
Prior to senescence, erythrocytes may, experience injury which compromises their integrity and thus triggers suicidal erythrocyte death or eryptosis. This mechanism is characterised by cell shrinkage, cell membrane blebbing, and cell membrane phospholipid scrambling after phosphatidylserine exposure on the cell surface that is identified by macrophages which engulf and degrade the eryptotic cells. The term eryptosis also includes typical mechanisms, which contribute to the triggering of this process. Among them: oxidative stress, Ca2+ entry with an increase in cytosolic Ca2+ activity ([Ca ]i) and the activation of p38 kinase, which is a kinase expressed in human erythrocytes and activated after hyperosmotic shock...
November 18, 2016: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/27791036/atm-g6pd-driven-redox-metabolism-promotes-flt3-inhibitor-resistance-in-acute-myeloid-leukemia
#15
Mark A Gregory, Angelo D'Alessandro, Francesca Alvarez-Calderon, Jihye Kim, Travis Nemkov, Biniam Adane, Andrii I Rozhok, Amit Kumar, Vijay Kumar, Daniel A Pollyea, Michael F Wempe, Craig T Jordan, Natalie J Serkova, Aik Choon Tan, Kirk C Hansen, James DeGregori
Activating mutations in FMS-like tyrosine kinase 3 (FLT3) are common in acute myeloid leukemia (AML) and drive leukemic cell growth and survival. Although FLT3 inhibitors have shown considerable promise for the treatment of AML, they ultimately fail to achieve long-term remissions as monotherapy. To identify genetic targets that can sensitize AML cells to killing by FLT3 inhibitors, we performed a genome-wide RNA interference (RNAi)-based screen that identified ATM (ataxia telangiectasia mutated) as being synthetic lethal with FLT3 inhibitor therapy...
October 25, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27711253/hspb1-enhances-sirt2-mediated-g6pd-activation-and-promotes-glioma-cell-proliferation
#16
Hongxing Ye, Hongguang Huang, Fei Cao, Mantao Chen, Xiujue Zheng, Renya Zhan
Heat shock proteins belong to a conserved protein family and are involved in multiple cellular processes. Heat shock protein 27 (Hsp27), also known as heat HSPB1, participates in cellular responses to not only heat shock, but also oxidative or chemical stresses. However, the contribution of HSPB1 to anti-oxidative response remains unclear. Here, we show that HSPB1 activates G6PD in response to oxidative stress or DNA damage. HSPB1 enhances the binding between G6PD and SIRT2, leading to deacetylation and activation of G6PD...
2016: PloS One
https://www.readbyqxmd.com/read/27684214/what-has-passed-is-prolog-new-cellular-and-physiological-roles-of-g6pd
#17
Hung-Chi Yang, Yi-Hsuan Wu, Hui-Ya Liu, Arnold Stern, Daniel Tsun-Yee Chiu
G6PD deficiency has been the most pervasive inherited disorder in the world since having been discovered. G6PD has an antioxidant role by functioning as a major nicotinamide adenine dinucleotide phosphate (NADPH) provider to reduce excessive oxidative stress. NADPH can produce reactive oxygen species (ROS) and reactive nitrogen species (RNS) mediated by NADPH oxidase (NOX) and nitric oxide synthase (NOS), respectively. Hence, G6PD also has a pro-oxidant role. Research in the past has focused on the enhanced susceptibility of G6PD-deficient cells or individuals to oxidative challenge...
October 2016: Free Radical Research
https://www.readbyqxmd.com/read/27660392/glutathione-depletion-pentose-phosphate-pathway-activation-and-hemolysis-in-erythrocytes-protecting-cancer-cells-from-vitamin-c-induced-oxidative-stress
#18
Zhuzhen Z Zhang, Eunice E Lee, Jessica Sudderth, Yangbo Yue, Ayesha Zia, Donald Glass, Ralph J Deberardinis, Richard C Wang
The discovery that oxidized vitamin C, dehydroascorbate (DHA), can induce oxidative stress and cell death in cancer cells has rekindled interest in the use of high dose vitamin C (VC) as a cancer therapy. However, high dose VC has shown limited efficacy in clinical trials, possibly due to the decreased bioavailability of oral VC. Because human erythrocytes express high levels of Glut1, take up DHA, and reduce it to VC, we tested how erythrocytes might impact high dose VC therapies. Cancer cells are protected from VC-mediated cell death when co-cultured with physiologically relevant numbers of erythrocytes...
October 28, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27636396/dexamethasone-improves-redox-state-in-ataxia-telangiectasia-cells-by-promoting-an-nrf2-mediated-antioxidant-response
#19
Sara Biagiotti, Michele Menotta, Sara Orazi, Chiara Spapperi, Serena Brundu, Alessandra Fraternale, Marzia Bianchi, Luigia Rossi, Luciana Chessa, Mauro Magnani
Ataxia telangiectasia (A-T) is a rare incurable neurodegenerative disease caused by biallelic mutations in the gene for ataxia-telangiectasia mutated (ATM). The lack of a functional ATM kinase leads to a pleiotropic phenotype, and oxidative stress is considered to have a crucial role in the complex physiopathology. Recently, steroids have been shown to reduce the neurological symptoms of the disease, although the molecular mechanism of this effect is largely unknown. In the present study, we have demonstrated that dexamethasone treatment of A-T lymphoblastoid cells increases the content of two of the most abundant antioxidants [glutathione (GSH) and NADPH] by up to 30%...
November 2016: FEBS Journal
https://www.readbyqxmd.com/read/27607238/vitamin-c-inhibits-aggravated-eryptosis-by-hydrogen-peroxide-in-glucose-6-phosphated-dehydrogenase-deficiency
#20
Feng Shan, Rui Yang, Tiemei Ji, Fengjun Jiao
BACKGROUND/AIMS: The study was aimed to investigate if vitamin C could exert protective effects on development of eryptosis caused by glucose-6-phosphate dehydrogenase (G6PD) deficiency and hydrogen peroxide. METHODS: Isolated erythrocytes with different G6PD activity (normal or deficient) were divided into various groups treated by either Vitamin C or H2O2. Phosphatidylserine (PS) extroversion rate was detected by Annexin V binding. The intracellular Ca2+ concentration was detected by Fluo3-fluorescence, and western blot was used to detect the expression of apoptosis factor caspase 3...
2016: Cellular Physiology and Biochemistry
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