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G6PD oxidative stress

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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
#1
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
#2
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...
December 30, 2016: Archives of Biochemistry and Biophysics
https://www.readbyqxmd.com/read/27981932/g6pd-deficiency-with-arnold-chiari-malformation
#3
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
#4
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
#5
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
#6
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
#7
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
#8
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
#9
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
#10
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
#11
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
#12
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
#13
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
#14
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
#15
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
https://www.readbyqxmd.com/read/27596070/oxidative-dna-damage-and-oxidative-stress-in-lead-exposed-workers
#16
M Dobrakowski, N Pawlas, A Kasperczyk, A Kozłowska, E Olewińska, A Machoń-Grecka, S Kasperczyk
There are many discrepancies among the results of studies on the genotoxicity of lead. The aim of the study was to explore lead-induced DNA damage, including oxidative damage, in relation to oxidative stress intensity parameters and the antioxidant defense system in human leukocytes. The study population consisted of 100 male workers exposed to lead. According to the blood lead (PbB) levels, they were divided into the following three subgroups: a group with PbB of 20-35 μg/dL (low exposure to lead (LE) group), a group with a PbB of 35-50 µg/dL (medium exposure to lead (ME) group), and a group with a PbB of >50 μg/dL (high exposure to lead (HE) group)...
September 5, 2016: Human & Experimental Toxicology
https://www.readbyqxmd.com/read/27450903/mirna-signatures-and-transcriptional-regulation-of-their-target-genes-in-vitiligo
#17
Mohmmad Shoab Mansuri, Mala Singh, Rasheedunnisa Begum
BACKGROUND: miRNAs are small non-coding RNA molecules that post-transcriptionally regulate gene expression. We have earlier reported the skin miRNA expression profiling in patients with non-segmental vitiligo. OBJECTIVE: In the present study, we show the expression of previously identified skin miRNAs signatures in blood and their target genes in whole blood and PBMCs as well as skin micro-environment of vitiligo patients and controls. METHODS: miRNA expression profiling in whole blood was performed using customized TaqMan(®) Low Density Array...
October 2016: Journal of Dermatological Science
https://www.readbyqxmd.com/read/27356773/aspirin-inhibits-glucose%C3%A2-6%C3%A2-phosphate-dehydrogenase-activity-in-hct-116-cells-through-acetylation-identification-of-aspirin-acetylated-sites
#18
Guoqiang Ai, Rakesh Dachineni, D Ramesh Kumar, Lloyd F Alfonso, Srinivasan Marimuthu, G Jayarama Bhat
Glucose-6-phosphate dehydrogenase (G6PD) catalyzes the first reaction in the pentose phosphate pathway, and generates ribose sugars, which are required for nucleic acid synthesis, and nicotinamide adenine dinucleotide phosphate (NADPH), which is important for neutralization of oxidative stress. The expression of G6PD is elevated in several types of tumor, including colon, breast and lung cancer, and has been implicated in cancer cell growth. Our previous study demonstrated that exposure of HCT 116 human colorectal cancer cells to aspirin caused acetylation of G6PD, and this was associated with a decrease in its enzyme activity...
August 2016: Molecular Medicine Reports
https://www.readbyqxmd.com/read/27284106/glucose-6-phosphate-dehydrogenase-deficiency-improves-insulin-resistance-with-reduced-adipose-tissue-inflammation-in-obesity
#19
Mira Ham, Sung Sik Choe, Kyung Cheul Shin, Goun Choi, Ji-Won Kim, Jung-Ran Noh, Yong-Hoon Kim, Je-Won Ryu, Kun-Ho Yoon, Chul-Ho Lee, Jae Bum Kim
Glucose-6-phosphate dehydrogenase (G6PD), a rate-limiting enzyme of the pentose phosphate pathway, plays important roles in redox regulation and de novo lipogenesis. It was recently demonstrated that aberrant upregulation of G6PD in obese adipose tissue mediates insulin resistance as a result of imbalanced energy metabolism and oxidative stress. It remains elusive, however, whether inhibition of G6PD in vivo may relieve obesity-induced insulin resistance. In this study we showed that a hematopoietic G6PD defect alleviates insulin resistance in obesity, accompanied by reduced adipose tissue inflammation...
September 2016: Diabetes
https://www.readbyqxmd.com/read/27241437/the-effect-of-experimental-thyroid-dysfunction-on-markers-of-oxidative-stress-in-rat-pancreas
#20
Mojtaba Sajadian, Mohammad Hashemi, Saeedeh Salimi, Alireza Nakhaee
Preclinical Research The aim of the present study was to evaluate the effects of thyroid dysfunction on markers of oxidative stress in rat pancreas. Hypothyroidism and hyperthyroidism were, respectively, induced in rats via administration of propylthiouracil (PTU) and L-thyroxine sodium salt in drinking water for 45 days. The activities of superoxide dismutase (SOD), catalase (CAT), glutathioen peroxidase (GPx), glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), xanthine oxidase (XO), and nonenzymatic markers of oxidative stress including malondialdehyde (MDA), protein carbonyl (PC), reduced glutathione (GSH), and total thiols (T-SH) were determined in the rat pancreas...
June 2016: Drug Development Research
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