scholarly journals Multiple strategies to prevent oxidative stress in Arabidopsis plants lacking the malate valve enzyme NADP-malate dehydrogenase

2011 ◽  
Vol 63 (3) ◽  
pp. 1445-1459 ◽  
Author(s):  
Inga Hebbelmann ◽  
Jennifer Selinski ◽  
Corinna Wehmeyer ◽  
Tatjana Goss ◽  
Ingo Voss ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Malate Dehydrogenase ◽  
Multiple Strategies ◽  
Malate Valve

scholarly journals Putative role of the malate valve enzyme NADP–malate dehydrogenase in H 2 O 2 signalling in Arabidopsis

2014 ◽  
Vol 369 (1640) ◽  
pp. 20130228 ◽  
Author(s):  
Eiri Heyno ◽  
Gilles Innocenti ◽  
Stéphane D. Lemaire ◽  
Emmanuelle Issakidis-Bourguet ◽  
Anja Krieger-Liszkay
Keyword(s):  
Malate Dehydrogenase ◽  
Catalase Activity ◽  
Redox State ◽  
Electron Flow ◽  
Light Stress ◽  
Reversible Inactivation ◽  
Photosynthetic Organisms ◽  
Cell Compartments ◽  
Malate Valve

In photosynthetic organisms, sudden changes in light intensity perturb the photosynthetic electron flow and lead to an increased production of reactive oxygen species. At the same time, thioredoxins can sense the redox state of the chloroplast. According to our hypothesis, thioredoxins and related thiol reactive molecules downregulate the activity of H 2 O 2 -detoxifying enzymes, and thereby allow a transient oxidative burst that triggers the expression of H 2 O 2 responsive genes. It has been shown recently that upon light stress, catalase activity was reversibly inhibited in Chlamydomonas reinhardtii in correlation with a transient increase in the level of H 2 O 2 . Here, it is shown that Arabidopsis thaliana mutants lacking the NADP–malate dehydrogenase have lost the reversible inactivation of catalase activity and the increase in H 2 O 2 levels when exposed to high light. The mutants were slightly affected in growth and accumulated higher levels of NADPH in the chloroplast than the wild-type. We propose that the malate valve plays an essential role in the regulation of catalase activity and the accumulation of a H 2 O 2 signal by transmitting the redox state of the chloroplast to other cell compartments.

scholarly journals Oxidative stress reversibly inactivates myocardial enzymes during cardiac arrest

2007 ◽  
Vol 292 (1) ◽  
pp. H198-H206 ◽  
Author(s):  
Arti B. Sharma ◽  
Jie Sun ◽  
Linda L. Howard ◽  
Arthur G. Williams ◽  
Robert T. Mallet
Keyword(s):  
Oxidative Stress ◽  
Creatine Kinase ◽  
Cardiac Arrest ◽  
Glutathione Reductase ◽  
Malate Dehydrogenase ◽  
Citrate Synthase ◽  
Left Ventricular ◽  
Partial Recovery ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Myocardial Enzymes

Oxidative stress during cardiac arrest may inactivate myocardial enzymes and thereby exacerbate ischemic derangements of myocardial metabolism. This study examined the impact of cardiac arrest on left ventricular enzymes. Beagles were subjected to 5 min of cardiac arrest and 5 min of open-chest cardiac compressions (OCCC) before epicardial direct current countershocks were applied to restore sinus rhythm. Glutathione/glutathione disulfide redox state (GSH/GSSG) and a panel of enzyme activities were measured in snap-frozen left ventricle. To test whether oxidative stress during arrest inactivated the enzymes, metabolic (pyruvate) or pharmacological ( N-acetyl-l-cysteine) antioxidants were infused intravenously for 30 min before arrest. During cardiac arrest, activities of phosphofructokinase, citrate synthase, aconitase, malate dehydrogenase, creatine kinase, glucose-6-phosphate dehydrogenase, and glutathione reductase fell by 56, 81, 55, 34, 42, 55, and 45%, respectively, coincident with 50% decline in GSH/GSSG. OCCC effected full recovery of glutathione reductase and partial recovery of citrate synthase and aconitase, in parallel with GSH/GSSG. Phosphofructokinase, malate dehydrogenase, creatine kinase, and glucose-6-phosphate dehydrogenase recovered only after cardioversion. Antioxidant pretreatments augmented phosphofructokinase, aconitase, and malate dehydrogenase activities before arrest and enhanced these activities, as well as those of citrate synthase and glucose-6-phosphate dehydrogenase, during arrest. In conclusion, cardiac arrest reversibly inactivates several important myocardial metabolic enzymes. Antioxidant protection of these enzymes implicates oxidative stress as a principal mechanism of enzyme inactivation during arrest.

scholarly journals Unlocking Survival Mechanisms for Metal and Oxidative Stress in the Extremely Acidophilic, Halotolerant Acidihalobacter Genus

Genes ◽  
2020 ◽  
Vol 11 (12) ◽  
pp. 1392
Author(s):  
Himel Nahreen Khaleque ◽  
Homayoun Fathollazadeh ◽  
Carolina González ◽  
Raihan Shafique ◽  
Anna H. Kaksonen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metal Tolerance ◽  
Acid Stress ◽  
Copper Resistance ◽  
Bioinformatic Tools ◽  
Multiple Strategies ◽  
Wide Range ◽  
Genes Encoding ◽  
Genomic Cluster ◽  
And Oxidative Stress

Microorganisms used for the biohydrometallurgical extraction of metals from minerals must be able to survive high levels of metal and oxidative stress found in bioleaching environments. The Acidihalobacter genus consists of four species of halotolerant, iron–sulfur-oxidizing acidophiles that are unique in their ability to tolerate chloride and acid stress while simultaneously bioleaching minerals. This paper uses bioinformatic tools to predict the genes and mechanisms used by Acidihalobacter members in their defense against a wide range of metals and oxidative stress. Analysis revealed the presence of multiple conserved mechanisms of metal tolerance. Ac. yilgarnensis F5T, the only member of this genus that oxidizes the mineral chalcopyrite, contained a 39.9 Kb gene cluster consisting of 40 genes encoding mobile elements and an array of proteins with direct functions in copper resistance. The analysis also revealed multiple strategies that the Acidihalobacter members can use to tolerate high levels of oxidative stress. Three of the Acidihalobacter genomes were found to contain genes encoding catalases, which are not common to acidophilic microorganisms. Of particular interest was a rubrerythrin genomic cluster containing genes that have a polyphyletic origin of stress-related functions.

scholarly journals Self-protection of cytosolic malate dehydrogenase against oxidative stress in Arabidopsis

2017 ◽  
Vol 69 (14) ◽  
pp. 3491-3505 ◽  
Author(s):  
Jingjing Huang ◽  
Adnan Khan Niazi ◽  
David Young ◽  
Leonardo Astolfi Rosado ◽  
Didier Vertommen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Malate Dehydrogenase ◽  
Self Protection ◽  
Cytosolic Malate Dehydrogenase

scholarly journals Investigation of serum isocitrate dehydrogenase, malate dehydrogenase and glutamate dehydrogenase activities with related oxidative stress markers in preeclampsia

2021 ◽  
Author(s):  
Sahabettin Selek ◽  
Ayse Zehra Gul ◽  
Nil Atakul ◽  
Sedat Meydan ◽  
Alime Sarıkaya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glutamate Dehydrogenase ◽  
Malate Dehydrogenase ◽  
Serum Levels ◽  
Stress Index ◽  
Photometric Method ◽  
Oxidative Markers ◽  
Novel Approach ◽  
Total Antioxidant ◽  
Underlying Mechanisms

Introduction: Preeclampsia, a high cause of fetomaternal morbidity-mortality, remains a significant burden affecting 8% of all pregnancies. Environmental conditions induce disease development leading to endothelial dysfunction in genetically predisposed women. Our aim is to discuss oxidative stress as a well-established contributing factor to disease progression with being the first study to show new evidence about serum dehydrogenase enzyme levels (isocitrate, malate, glutamate dehydrogenase) with oxidative markers (myeloperoxidase, total antioxidant-oxidant status, oxidative stress index). Methods: Serum parameters were analyzed with photometric method (Abbott ARCHITECT c8000). Results: Results showed that the enzyme levels and oxidative markers were significantly higher in patients, supporting the redox imbalance in preeclampsia. According to ROC analysis, malate dehydrogenase showed an outstanding diagnostic ability with the highest AUC value of 0.9 and the cut-off value of 51.2 IU/L. Discriminant analysis including malate, isocitrate and glutamate dehydrogenase had predicted preeclampsia with an overall %87.9 accuracy. Discussion: Considering the above results, we propose that the enzyme levels increase with oxidative stress functioning as antioxidant defense factors. The unique finding of the study is that the serum levels of malate, isocitrate and glutamate dehydrogenase can be used both separately and combined in the early prediction of preeclampsia. As a novel approach, we also offer combining serum isocitrate and glutamate dehydrogenase levels with ALT, AST tests to state liver functions more reliably in patients. Still, larger sample-sized studies investigating enzyme expression levels are required to confirm the recent findings and to reveal underlying mechanisms.

Lycopene alleviates sulfamethoxazole-induced hepatotoxicity in grass carp (Ctenopharyngodon idellus) via suppression of oxidative stress, inflammation and apoptosis

2020 ◽  
Vol 11 (10) ◽  
pp. 8547-8559
Author(s):  
Hongjing Zhao ◽  
Yu Wang ◽  
Mengyao Mu ◽  
Menghao Guo ◽  
Hongxian Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Secondary Metabolites ◽  
Human Health ◽  
Grass Carp ◽  
Aquatic Environment ◽  
Ctenopharyngodon Idellus

Antibiotics are used worldwide to treat diseases in humans and other animals; most of them and their secondary metabolites are discharged into the aquatic environment, posing a serious threat to human health.

Copper-dependent ATP7B up-regulation drives the resistance of TMEM16A-overexpressing head-and-neck cancer models to platinum toxicity

2019 ◽  
Vol 476 (24) ◽  
pp. 3705-3719 ◽  
Author(s):  
Avani Vyas ◽  
Umamaheswar Duvvuri ◽  
Kirill Kiselyov
Keyword(s):  
Oxidative Stress ◽  
Head And Neck ◽  
Transcriptional Activation ◽  
Platinum Resistance ◽  
Mrna Levels ◽  
Strong Positive Correlation ◽  
Platinum Compounds ◽  
Copper Chelation ◽  
Novel Approach ◽  
Cancer Models

Platinum-containing drugs such as cisplatin and carboplatin are routinely used for the treatment of many solid tumors including squamous cell carcinoma of the head and neck (SCCHN). However, SCCHN resistance to platinum compounds is well documented. The resistance to platinum has been linked to the activity of divalent transporter ATP7B, which pumps platinum from the cytoplasm into lysosomes, decreasing its concentration in the cytoplasm. Several cancer models show increased expression of ATP7B; however, the reason for such an increase is not known. Here we show a strong positive correlation between mRNA levels of TMEM16A and ATP7B in human SCCHN tumors. TMEM16A overexpression and depletion in SCCHN cell lines caused parallel changes in the ATP7B mRNA levels. The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS). Pretreatment with either chelator significantly increased cisplatin's sensitivity, particularly in the context of TMEM16A overexpression. We propose that increased oxidative stress in TMEM16A-overexpressing cells liberates the chelated copper in the cytoplasm, leading to the transcriptional activation of ATP7B expression. This, in turn, decreases the efficacy of platinum compounds by promoting their vesicular sequestration. We think that such a new explanation of the mechanism of SCCHN tumors’ platinum resistance identifies novel approach to treating these tumors.

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

Pancreatic stones shockwave lithotripsy induces oxidative stress. A study of lipoperoxidation products in pure pancreatic juice

2001 ◽  
Vol 120 (5) ◽  
pp. A217-A217
Author(s):  
C SPADA ◽  
S SANTINI ◽  
F FOSCHIA ◽  
M PANDOLFI ◽  
V PERRI ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pancreatic Juice ◽  
Shockwave Lithotripsy ◽  
Pure Pancreatic Juice ◽  
Pancreatic Stones
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