Upregulation of glucose-6-phosphate dehydrogenase in response to hepatocellular oxidative stress: Studies with diquat

Ochratoxin A (OTA) is a mycotoxin that is potentially carcinogenic to humans. Although its mechanism remains unclear, oxidative stress has been recognized as a plausible cause for the potent renal carcinogenicity observed in experimental animals. The effect of OTA on oxidative stress parameters in two cell lines of LLC-PK1 and HK-2 derived from the kidneys of pig and human, respectively, were investigated and compared. We found that the cytotoxicity of OTA on LLC-PK1 and HK-2 cells was dose- and time-dependent in both cell lines. Furthermore, increased intracellular reactive oxygen species (ROS) induced by OTA in both cell lines were observed in a time-dependent manner. Glutathione (GSH) was depleted by OTA at >48 h in HK-2 but not in LLC-PK1 cells. While the mRNA levels of glucose-6-phosphate dehydrogenase (G6PD) and glutathione peroxidase 1 (GPX1) in LLC-PK1 were down-regulated by 0.67- and 0.66-fold, respectively, those of catalase (CAT), glutathione reductase (GSR), and superoxide dismutase 1 (SOD) in HK-2 were up-regulated by 2.20-, 2.24-, and 2.75-fold, respectively, after 72 h exposure to OTA. Based on these results, we conclude that HK-2 cells are more sensitive to OTA-mediated toxicity than LLC-PK1, and OTA can cause a significant oxidative stress in HK-2 as indicated by changes in the parameter evaluated.

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Eugenol attenuates concanavalin A-induced hepatitis through modulation of cytokine levels and inhibition of mitochondrial oxidative stress

Archives of Biological Sciences ◽

10.2298/abs190121016l ◽

2019 ◽

Vol 71 (2) ◽

pp. 339-346

Author(s):

Jing Liu ◽

Yidong Mao

Keyword(s):

Oxidative Stress ◽

Concanavalin A ◽

Hepatoprotective Activity ◽

Antioxidant Enzyme Activities ◽

Mitochondrial Oxidative Stress ◽

Immune Mediated ◽

Wide Range ◽

Cytokine Levels ◽

Glucose 6 Phosphate Dehydrogenase

Therapeutic management of hepatitis with conventional drugs alone worsens hepatic functioning in the long term because of sustained oxidative stress. Active compounds from several plant sources have been investigated to counteract this. Eugenol, a phytochemical abundant in various plants, is known for its wide range of pharmacological effects. There is a lacuna in the deeper understanding of its hepatoprotective activity at the molecular level. Our present study aimed to determine the effects of eugenol on the changes in antioxidant components, inflammatory cytokines and modulation of mitochondrial oxidative stress in immune-mediated hepatitis. We employed a model that mimics viral hepatitis using concanavalin A (ConA) to induce T-cell-mediated acute hepatitis. Eugenol increased (P<0.01) antioxidant enzyme activities, including reduced glutathione (GSH)-regenerating enzyme, glutathione reductase, and glucose-6-phosphate dehydrogenase. Its antiinflammatory and antifibrogenic effects were evident from the reduction (P<0.01) in interleukin and tumor necrosis factor levels. Eugenol was found to decrease mitochondrial oxidative stress, which was elevated in hepatitis. The hepatoprotective effects of eugenol were confirmed by histological findings. The current investigation shows that eugenol exerts a hepatoprotective effect through the modulation of different pathways which include restoration of mitochondrial oxidative stress. Eugenol could be a promising candidate for human hepatitis management, warranting preclinical studies.

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A Rare Case of Coexistence of Homozygous β-Thalassaemia and Glucose 6 Phosphate Dehydrogenase Deficiency

JOURNAL FOR CLINICAL AND DIAGNOSTIC RESEARCH ◽

10.7860/jcdr/2020/44968.14085 ◽

2020 ◽

Author(s):

Jitendar Mohan Khunger ◽

Monika Gupta ◽

Ankur Jain ◽

Monica Khunger Malhotra

Keyword(s):

Oxidative Stress ◽

Blood Cells ◽

G6pd Deficiency ◽

Rare Case ◽

Dehydrogenase Deficiency ◽

Globin Gene ◽

Genetic Abnormality ◽

Wide Range ◽

Symptomatic Anaemia ◽

Glucose 6 Phosphate Dehydrogenase

β-thalassaemia is one of the most prevalent autosomal disorders worldwide. Mutations/deletions in globin gene underlie deficiencies in Haemoglobin (Hb) production, which can interfere with oxygen delivery by Hb, resulting in thalassaemias causing anaemias with a wide range of disease severity. Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is a genetic abnormality resulting in inadequate amount of G6PD in the Red Blood Cells (RBCs). In patients with G6PD deficiency, the reduced or absent activity of the enzyme in RBCs causes premature haemolysis and symptomatic anaemia. The marked oxidative stress caused by homozygous β-thalassaemia is apparently incompatible with G6PD deficiency. Here, a rare case of six-month-old male child is described who presented with severe pallor hepato-splenomegaly and these two conditions co-existed in this patient.

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Relationship between Type 2 Diabetes and Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency and Their Effect on Oxidative Stress

Journal of Diabetes & Metabolism ◽

10.4172/2155-6156.1000800 ◽

2018 ◽

Vol 09 (08) ◽

Cited By ~ 1

Author(s):

Godwill Azeh Engwa ◽

Friday Nweke Nwalo ◽

Gregory Eze Chibuzor ◽

Endaline Chiamaka Ejiagha ◽

Micheal Chinweuba Abonyi ◽

...

Keyword(s):

Oxidative Stress ◽

Type 2 Diabetes ◽

G6pd Deficiency ◽

Glucose 6 Phosphate Dehydrogenase

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Paroxysmal Nocturnal Hemoglobinuria with Glucose-6-Phosphate Dehydrogenase Deficiency: A Case Report and Review of the Literature

Case Reports in Oncology ◽

10.1159/000503817 ◽

2019 ◽

Vol 12 (3) ◽

pp. 838-844

Author(s):

Mahmoud S. Eisa ◽

Shehab F. Mohamed ◽

Firyal Ibrahim ◽

Khalid Shariff ◽

Nagham Sadik ◽

...

Keyword(s):

Oxidative Stress ◽

G6pd Deficiency ◽

Paroxysmal Nocturnal Hemoglobinuria ◽

Dehydrogenase Deficiency ◽

Response To Treatment ◽

X Chromosomes ◽

Financial Status ◽

Glucose 6 Phosphate Dehydrogenase ◽

Real Challenge ◽

And Oxidative Stress

In this study, we are describing a female patient with paroxysmal nocturnal hemoglobinuria (PNH) and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Both diseases are known to cause hemolytic anemia that mediates the hemolysis of RBCs through several mechanisms. In PNH the hemolysis is mediated through complement activation and oxidative stress. G6PD enzyme is crucial in preventing damage to cellular structures caused by oxygen-free radicles. In G6PD deficiency the hemolysis is mediated through the oxidative stress created by oxygen-free radicles. Since both diseases mediate hemolysis through the oxidative stress, we hypothesize that both conditions have facilitated an effect on each other and this will reflect on the response to treatment, and this response to treatment could vary based on whether the two mutations occurred in the same gene or in two different X chromosomes. Having diagnosed PNH, the management is very expensive and not all the patients can afford it, especially our patient who is a maid by occupation. So, the real challenge in our case is to monitor her in subsequent visits and to plan the treatment keeping in mind her financial status.

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Identification, Characterization, and Stress Responsiveness of Glucose-6-phosphate Dehydrogenase Genes in Highland Barley

Plants ◽

10.3390/plants9121800 ◽

2020 ◽

Vol 9 (12) ◽

pp. 1800

Author(s):

Ruijun Feng ◽

Xiaomin Wang ◽

Li He ◽

Shengwang Wang ◽

Junjie Li ◽

...

Keyword(s):

Oxidative Stress ◽

Redox Homeostasis ◽

Nicotinamide Adenine Dinucleotide Phosphate ◽

Reducing Power ◽

Cellular Redox ◽

E Coli ◽

Intermediate Metabolites ◽

Glucose 6 Phosphate Dehydrogenase ◽

Highland Barley ◽

Salt And Drought Stresses

G6PDH provides intermediate metabolites and reducing power (nicotinamide adenine dinucleotide phosphate, NADPH) for plant metabolism, and plays a pivotal role in the cellular redox homeostasis. In this study, we cloned five G6PDH genes (HvG6PDH1 to HvG6PDH5) from highland barley and characterized their encoded proteins. Functional analysis of HvG6PDHs in E. coli showed that HvG6PDH1 to HvG6PDH5 encode the functional G6PDH proteins. Subcellular localization and phylogenetic analysis indicated that HvG6PDH2 and HvG6PDH5 are localized in the cytoplasm, while HvG6PDH1, HvG6PDH3, and HvG6PDH4 are plastidic isoforms. Analysis of enzymatic activities and gene expression showed that HvG6PDH1 to HvG6PDH4 are involved in responses to salt and drought stresses. The cytosolic HvG6PDH2 is the major isoform against oxidative stress. HvG6PDH5 may be a house-keeping gene. In addition, HvG6PDH1 to HvG6PDH4 and their encoded enzymes responded to jasmonic acid (JA) and abscisic acid (ABA) treatments, implying that JA and ABA are probably critical regulators of HvG6PDHs (except for HvG6PDH5). Reactive oxygen species analysis showed that inhibition of cytosolic and plastidic G6PDH activities leads to increased H2O2 and O2− contents in highland barley under salt and drought stresses. These results suggest that G6PDH can maintain cellular redox homeostasis and that cytosolic HvG6PDH2 is an irreplaceable isoform against oxidative stress in highland barley.

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Oxidative stress induced by torsion of the spermatic cord in young rats

Acta Cirurgica Brasileira ◽

10.1590/s0102-86502007000100005 ◽

2007 ◽

Vol 22 (1) ◽

pp. 30-33 ◽

Cited By ~ 12

Author(s):

Sergio Botelho Guimarães ◽

Alan Arruda Aragão ◽

Jefferson Menezes Viana Santos ◽

Osamu de Sandes Kimura ◽

Paulo Hudson Uchoa Barbosa ◽

...

Keyword(s):

Oxidative Stress ◽

Spermatic Cord ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Sham Operation ◽

Additional Increase ◽

Antioxidant Power ◽

Spermatic Cord Torsion ◽

Stress Studies ◽

Male Wistar Rats

PURPOSE: To evaluate the effects of the oxidative stress in an experimental model of torsion/detorsion of the spermatic cord and the legitimacy of this model for oxidative stress studies. METHODS: Forty-eight male Wistar rats were randomized in two groups (n=24): G-1 (Sham) and G-2 (Ischemia/Reperfusion). All rats received intraperitoneal saline injections (2.0 ml), at 21, 9, and 1 h before right spermatic cord torsion or first sham operation. Detorsion or second sham operation was carried out 3 h later followed by testis and blood samples collection (T-0). Additional samples were collected at 1-3-6 h time-points for assessment of testis malonaldehyde, glutathione, and plasma total antioxidant power (TAP). RESULTS: Spermatic cord torsion/detorsion induced a significant increase in testicular malonaldehyde contents and a significant decrease in glutathione concentrations in ischemic rats compared with sham animals. Additional increase in malonaldehyde levels occurred during reperfusion in G-2 rats. TAP was similar in both groups denoting absence of systemic effects in this study. CONCLUSION: Torsion/detorsion of the spermatic cord for 3 h induces significant lipid peroxidation and reduction in glutathione content of the testis and is, therefore, a valid model for studying the oxidative stress effects of the ischemia/reperfusion injury in young rat testis.

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