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G6PD oxidative stress

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
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 NADPH provider to reduce excessive oxidative stress. NADPH can produce reactive oxygen species and reactive nitrogen species 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...
August 10, 2016: Free Radical Research
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, dehy-droascorbate (DHA), can induce oxidative stress and cell death in cancer cells has rekindled in-terest 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...
September 22, 2016: Journal of Biological Chemistry
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%...
September 16, 2016: FEBS Journal
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
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
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
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
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
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
Anna D Cunningham, Sunhee Hwang, Daria Mochly-Rosen
Hyperbilirubinemia occurs frequently in newborns, and in severe cases can progress to kernicterus and permanent developmental disorders. Glucose-6-phosphate dehydrogenase (G6PD) deficiency, one of the most common human enzymopathies, is a major risk factor for hyperbilirubinemia and greatly increases the risk of kernicterus even in the developed world. Therefore, a novel treatment for kernicterus is needed, especially for G6PD-deficient newborns. Oxidative stress is a hallmark of bilirubin toxicity in the brain...
June 2016: Clinics in Perinatology
Kelei Dong, Hua Ni, Meiling Wu, Ziqing Tang, Michael Halim, Dongyun Shi
Oxidative stress is known to contribute to insulin resistance in diabetes, however the mechanism is not clear. Here we show that reactive oxygen species (ROS) could reprogram the glucose metabolism through upregulating the pentose pathway so as to induce insulin resistance in type 2 diabetes (T2DM). By using streptozotocin-high fat diet (STZ-HFD) induced T2DM in rats, we show that diabetic rats exhibited high level of oxidative stress accompanied with insulin resistance. Hypoxia inducible factor (HIF-1α) protein expression as well as its downstream target glucokinase (GK), were upregulated; The glycogen synthesis increased accordingly; However the glycolysis was inhibited as indicated by decreased phosphofructokinase-1 (PFK-1), pyruvate kinase (PK), phospho-PFK-2/PFK-2 (p-PFK-2/PFK-2) ratio, lactate dehydrogenase (LDH) and pyruvate dehydrogenase kinase (PDK); Pyruvate dehydrogenase (PDH) which promotes pyruvate to generate acetyl-CoA declined as well...
August 5, 2016: Biochemical and Biophysical Research Communications
Lisha Zhou, Fang Wang, Renqiang Sun, Xiufei Chen, Mengli Zhang, Qi Xu, Yi Wang, Shiwen Wang, Yue Xiong, Kun-Liang Guan, Pengyuan Yang, Hongxiu Yu, Dan Ye
Excess in mitochondrial reactive oxygen species (ROS) is considered as a major cause of cellular oxidative stress. NADPH, the main intracellular reductant, has a key role in keeping glutathione in its reduced form GSH, which scavenges ROS and thus protects the cell from oxidative damage. Here, we report that SIRT5 desuccinylates and deglutarylates isocitrate dehydrogenase 2 (IDH2) and glucose-6-phosphate dehydrogenase (G6PD), respectively, and thus activates both NADPH-producing enzymes. Moreover, we show that knockdown or knockout of SIRT5 leads to high levels of cellular ROS SIRT5 inactivation leads to the inhibition of IDH2 and G6PD, thereby decreasing NADPH production, lowering GSH, impairing the ability to scavenge ROS, and increasing cellular susceptibility to oxidative stress...
June 2016: EMBO Reports
Hsin-Ru Lin, Yi-Hsuan Wu, Wei-Chen Yen, Chuen-Mao Yang, Daniel Tsun-Yee Chiu
Glucose-6-phosphate dehydrogenase (G6PD) provides the reducing agent NADPH to meet the cellular needs for reductive biosynthesis and the maintenance of redox homeostasis. G6PD-deficient cells experience a high level of oxidative stress and an increased susceptibility to viral infections. Cyclooxygenase-2 (COX-2) is a key mediator in the regulation of viral replication and inflammatory response. In the current study, the role of G6PD on the inflammatory response was determined in both scramble control and G6PD-knockdown (G6PD-kd) A549 cells upon tumor necrosis factor-α (TNF-α) stimulation...
2016: PloS One
Vassilis L Tzounakas, Anastasios G Kriebardis, Hara T Georgatzakou, Leontini E Foudoulaki-Paparizos, Monika Dzieciatkowska, Matthew J Wither, Travis Nemkov, Kirk C Hansen, Issidora S Papassideri, Angelo D'Alessandro, Marianna H Antonelou
Storage of packed red blood cells (RBCs) is associated with progressive accumulation of lesions, mostly triggered by energy and oxidative stresses, which potentially compromise the effectiveness of the transfusion therapy. Concerns arise as to whether glucose 6-phosphate dehydrogenase deficient subjects (G6PD(-)), ~5% of the population in the Mediterranean area, should be accepted as routine donors in the light of the increased oxidative stress their RBCs suffer from. To address this question, we first performed morphology (scanning electron microscopy), physiology and omics (proteomics and metabolomics) analyses on stored RBCs from healthy or G6PD(-) donors...
July 2016: Free Radical Biology & Medicine
Xu Wang, Yijie Bai, Guyue Cheng, Awais Ihsan, Feng Zhu, Yulian Wang, Yanfei Tao, Dongmei Chen, Menghong Dai, Zhengli Liu, Zonghui Yuan
Quinoxaline 1,4-dioxides (QdNOs) are widely used as a kind of antibacterial growth promoter in animal husbandry. The adrenal cortex was found to be one of the main toxic targets of QdNOs, accompanied by a decreased aldosterone level. However, the way in which QdNOs decrease production of the hormone aldosterone is far from clear. To illustrate the mechanism by which QdNOs damage the adrenal cortex and decrease aldosterone hormone levels, the QdNOs were screened to choose the drug with most toxic effects on aldosterone production, and then to reveal the mechanism between the gene and protein profiles in human adrenocortical cells (NCI-H295R cells)...
March 28, 2016: Toxicology
Man Xiao, Guankui Du, Guobing Zhong, Dongjing Yan, Huazong Zeng, Wangwei Cai
Favism is a life-threatening hemolytic anemia resulting from the intake of fava beans by susceptible individuals with low erythrocytic glucose 6-phosphate dehydrogenase (G6PD) activity. However, little is known about the metabolomic changes in plasma and liver after the intake of fava beans in G6PD normal and deficient states. In this study, gas chromatography/mass spectrometry was used to analyze the plasma and liver metabolic alterations underlying the effects of fava beans in C3H- and G6PD-deficient (G6PDx) mice, and to find potential biomarkers and metabolic changes associated with favism...
2016: PloS One
Mohammed Zeeshan, Anbazhagan Murugadas, Surendra Ghaskadbi, Ramasamy Babu Rajendran, Mohammad Abdulkader Akbarsha
Copper, an essential microelement, is known to be toxic to aquatic life at concentrations higher than that could be tolerated. Copper-induced oxidative stress has been documented in vitro, yet the in vivo effects of metal-induced oxidative stress have not been extensively studied in the lower invertebrates. The objective of the present study has been to find the effect of ROS-mediated toxicity of environmentally relevant concentrations of copper at organismal and cellular levels in Hydra magnipapillata. Exposure to copper at sublethal concentrations (0...
July 2016: Comparative Biochemistry and Physiology. Toxicology & Pharmacology: CBP
William D Cameron, Cindy V Bui, Ashley Hutchinson, Peter Loppnau, Susanne Gräslund, Jonathan V Rocheleau
NADPH-dependent antioxidant pathways have a critical role in scavenging hydrogen peroxide (H2O2) produced by oxidative phosphorylation. Inadequate scavenging results in H2O2 accumulation and can cause disease. To measure NADPH/NADP(+) redox states, we explored genetically encoded sensors based on steady-state fluorescence anisotropy due to FRET (fluorescence resonance energy transfer) between homologous fluorescent proteins (homoFRET); we refer to these sensors as Apollo sensors. We created an Apollo sensor for NADP(+) (Apollo-NADP(+)) that exploits NADP(+)-dependent homodimerization of enzymatically inactive glucose-6-phosphate dehydrogenase (G6PD)...
April 2016: Nature Methods
Pawan Kumar Maurya, Prabhanshu Kumar, Pranjal Chandra
CONTEXT: Glucose-6-phosphate dehydrogenase (G6PD) is an important enzyme of hexose monophosphate shunt, involved in the biosynthesis of reduced nicotinamide adenine dinucleotide phosphate hydrogen (NADPH). OBJECTIVE: This study was designed to investigate age-dependent changes in human erythrocyte G6PD activity. The G6PD activity pattern was correlated with reduced glutathione (GSH) and total antioxidant potential in terms of FRAP (ferric reducing ability of plasma) value...
2016: Archives of Physiology and Biochemistry
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