Identifying the Predictive Role of Oxidative Stress Genes in the Prognosis of Glioma Patients

Objective. Neonates have a high risk of oxidative stress during anesthetic procedures. The predictive role of oxidative stress biomarkers on the occurrence of brain injury in the perioperative period has not been reported before. Methods. A prospective cohort study of patients requiring major surgery in the neonatal period was conducted. Biomarker levels of nonprotein-bound iron (NPBI) in plasma and F2-isoprostane in plasma and urine before and after surgical intervention were determined. Brain injury was assessed using postoperative MRI. Results. In total, 61 neonates were included, median gestational age at 39 weeks (range 31–42) and weight at 3000 grams (1400–4400). Mild to moderate brain lesions were found in 66%. Logistic regression analysis showed a significant difference between plasma NPBI in patients with nonparenchymal injury versus no brain injury: 1.34 umol/L was identified as correlation threshold for nonparenchymal injury (sensitivity 67%, specificity 91%). In the multivariable analysis, correcting for GA, no other significant relation was found with the oxidative stress biomarkers and risk factors. Conclusion. Oxidative stress seems to occur during anaesthesia in this cohort of neonates. Plasma nonprotein-bound iron showed to be associated with nonparenchymal injury after surgery, with values of 1.34 umol/L or higher. Risk factors should be elucidated in a more homogeneous patient group.

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Role of the Hog1 Stress-activated Protein Kinase in the Global Transcriptional Response to Stress in the Fungal PathogenCandida albicans

Molecular Biology of the Cell ◽

10.1091/mbc.e05-06-0501 ◽

2006 ◽

Vol 17 (2) ◽

pp. 1018-1032 ◽

Cited By ~ 253

Author(s):

Brice Enjalbert ◽

Deborah A. Smith ◽

Michael J. Cornell ◽

Intikhab Alam ◽

Susan Nicholls ◽

...

Keyword(s):

Oxidative Stress ◽

Heavy Metal ◽

Protein Kinase ◽

Transcriptional Response ◽

Heavy Metal Stress ◽

Transcriptional Responses ◽

Stress Genes ◽

The Core ◽

Response To Stress

The resistance of Candida albicans to many stresses is dependent on the stress-activated protein kinase (SAPK) Hog1. Hence we have explored the role of Hog1 in the regulation of transcriptional responses to stress. DNA microarrays were used to characterize the global transcriptional responses of HOG1 and hog1 cells to three stress conditions that activate the Hog1 SAPK: osmotic stress, oxidative stress, and heavy metal stress. This revealed both stress-specific transcriptional responses and a core transcriptional response to stress in C. albicans. The core transcriptional response was characterized by a subset of genes that responded in a stereotypical manner to all of the stresses analyzed. Inactivation of HOG1 significantly attenuated transcriptional responses to osmotic and heavy metal stresses, but not to oxidative stress, and this was reflected in the role of Hog1 in the regulation of C. albicans core stress genes. Instead, the Cap1 transcription factor plays a key role in the oxidative stress regulation of C. albicans core stress genes. Our data show that the SAPK network in C. albicans has diverged from corresponding networks in model yeasts and that the C. albicans SAPK pathway functions in parallel with other pathways to regulate the core transcriptional response to stress.

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Role of Genetic Variants in Immunoregulatory and Oxidative Stress Genes with Predisposition to Pre-eclampsia: A possibility for Predicting the High Risks in Synergetic Reaction

Bioscience Biotechnology Research Communications ◽

10.21786/bbrc/12.3/5 ◽

2019 ◽

Vol 12 (3) ◽

pp. 584-589

Author(s):

Safia Begum ◽

Hafsa Ambareen ◽

Mohd Ishaq ◽

Parveen Nyamath ◽

Imran Ali Khan

Keyword(s):

Oxidative Stress ◽

Genetic Variants ◽

Stress Genes ◽

And Oxidative Stress

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The role of oxidative stress genes and effect of pH on methylene blue sensitized photooxidation ofEscherichia coli

Acta Biologica Hungarica ◽

10.1556/018.67.2016.1.7 ◽

2016 ◽

Vol 67 (1) ◽

pp. 85-98 ◽

Cited By ~ 1

Author(s):

Önder İdil ◽

İkbal Macit ◽

Özge Kaygusuz ◽

Cihan Darcan

Keyword(s):

Oxidative Stress ◽

Methylene Blue ◽

Ofescherichia Coli ◽

Effect Of Ph ◽

Stress Genes

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NRF2 Protection against Liver Injury Produced by Various Hepatotoxicants

Oxidative Medicine and Cellular Longevity ◽

10.1155/2013/305861 ◽

2013 ◽

Vol 2013 ◽

pp. 1-8 ◽

Cited By ~ 64

Author(s):

Jie Liu ◽

Kai Connie Wu ◽

Yuan-Fu Lu ◽

Edugie Ekuase ◽

Curtis D. Klaassen

Keyword(s):

Oxidative Stress ◽

Liver Injury ◽

Fas Ligand ◽

Inflammatory Responses ◽

Lithocholic Acid ◽

Antioxidant Genes ◽

Stress Genes ◽

Nrf2 Activation ◽

Genes Encoding

To investigate the role of Nrf2 as a master defense against the hepatotoxicity produced by various chemicals, Nrf2-null, wild-type, Keap1-knock down (Keap1-Kd) and Keap1-hepatocyte knockout (Keap1-HKO) mice were used as a “graded Nrf2 activation” model. Mice were treated with 14 hepatotoxicants at appropriate doses, and blood and liver samples were collected thereafter (6 h to 7 days depending on the hepatotoxicant). Graded activation of Nrf2 offered a Nrf2-dependent protection against the hepatotoxicity produced by carbon tetrachloride, acetaminophen, microcystin, phalloidin, furosemide, cadmium, and lithocholic acid, as evidenced by serum alanine aminotransferase (ALT) activities and by histopathology. Nrf2 activation also offered moderate protection against liver injury produced by ethanol, arsenic, bromobenzene, and allyl alcohol but had no effects on the hepatotoxicity produced by D-galactosamine/endotoxin and the Fas ligand antibody Jo-2. Graded Nrf2 activation reduced the expression of inflammatory genes (MIP-2, mKC, IL-1β, IL-6, and TNFα), oxidative stress genes (Ho-1, Egr1), ER stress genes (Gadd45 and Gadd153), and genes encoding cell death (Noxa, Bax, Bad, and caspase3). Thus, this study demonstrates that Nrf2 prevents the liver from many, but not all, hepatotoxicants. The Nrf2-mediated protection is accompanied by induction of antioxidant genes, suppression of inflammatory responses, and attenuation of oxidative stress.

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Expression of Reactive Oxygen Species–Related Transcripts in Egyptian Children With Autism

Biomarker Insights ◽

10.1177/1177271917691035 ◽

2017 ◽

Vol 12 ◽

pp. 117727191769103 ◽

Cited By ~ 9

Author(s):

Nagwa A Meguid ◽

Said A S Ghozlan ◽

Magda F Mohamed ◽

Marwa K Ibrahim ◽

Reham M Dawood ◽

...

Keyword(s):

Oxidative Stress ◽

Healthy Subjects ◽

Pcr Array ◽

Peripheral Blood Mononuclear ◽

Stress Genes ◽

Diagnosis And Prognosis ◽

Egyptian Children ◽

Transcriptional Pattern ◽

Pathophysiological Role

The molecular basis of the pathophysiological role of oxidative stress in autism is understudied. Herein, we used polymerase chain reaction (PCR) array to analyze transcriptional pattern of 84 oxidative stress genes in peripheral blood mononuclear cell pools isolated from 32 autistic patients (16 mild/moderate and 16 severe) and 16 healthy subjects (each sample is a pool from 4 autistic patients or 4 controls). The PCR array data were further validated by quantitative real-time PCR in 80 autistic children (55 mild/moderate and 25 severe) and 60 healthy subjects. Our data revealed downregulation in GCLM, SOD2, NCF2, PRNP, and PTGS2 transcripts (1.5, 3.8, 1.2, 1.7, and 2.2, respectively; P < .05 for all) in autistic group compared with controls. In addition, TXN and FTH1 exhibited 1.4- and 1.7-fold downregulation, respectively, in severe autistic patients when compared with mild/moderate group ( P = .005 and .0008, respectively). This study helps in a better understanding of the underlying biology and related genetic factors of autism, and most importantly, it presents suggested candidate biomarkers for diagnosis and prognosis purposes as well as targets for therapeutic intervention.

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Transcription of Oxidative Stress Genes Is Directly Activated by SpxA1 and, to a Lesser Extent, by SpxA2 in Streptococcus mutans

Journal of Bacteriology ◽

10.1128/jb.00118-15 ◽

2015 ◽

Vol 197 (13) ◽

pp. 2160-2170 ◽

Cited By ~ 24

Author(s):

Jessica K. Kajfasz ◽

Isamar Rivera-Ramos ◽

Kathleen Scott-Anne ◽

Stacy Gregoire ◽

Jacqueline Abranches ◽

...

Keyword(s):

Oxidative Stress ◽

Oral Cavity ◽

Streptococcus Mutans ◽

Stress Responses ◽

Dominant Role ◽

Critical Role ◽

Content Type ◽

Stress Genes

ABSTRACTThe SpxA1 and SpxA2 (formerly SpxA and SpxB) transcriptional regulators ofStreptococcus mutansare members of a highly conserved family of proteins found inFirmicutes, and they were previously shown to activate oxidative stress responses. In this study, we showed that SpxA1 exerts substantial positive regulatory influence over oxidative stress genes following exposure to H2O2, while SpxA2 appears to have a secondary regulatory role.In vitrotranscription (IVT) assays using purified SpxA1 and/or SpxA2 showed that SpxA1 and, less often, SpxA2 directly activate transcription of some of the major oxidative stress genes. Addition of equimolar concentrations of SpxA1 and SpxA2 to the IVT reactions neither enhanced transcription of the tested genes nor disrupted the dominant role of SpxA1. Substitution of a conserved glycine residue (G52) present in both Spx proteins by arginine (SpxG52R) resulted in strains that phenocopied the Δspxstrains. Moreover, addition of purified SpxA1G52Rcompletely failed to activate transcription ofahpC,sodA, andtpx, further confirming that the G52 residue is critical for Spx functionality.IMPORTANCEStreptococcus mutansis a pathogen associated with the formation of dental caries in humans. Within the oral cavity,S. mutansroutinely encounters oxidative stress. Our previous data revealed that two regulatory proteins, SpxA1 and SpxA2 (formerly SpxA and SpxB), bear high homology to the Spx regulator that has been characterized as a critical activator of oxidative stress genes inBacillus subtilis. In this report, we prove that Spx proteins ofS. mutansdirectly activate transcription of genes involved in the oxidative stress response, though SpxA1 appears to have a more dominant role than SpxA2. Therefore, the Spx regulators play a critical role in the ability ofS. mutansto thrive within the oral cavity.

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LIN-35 beyond its classical roles: its function in the stress response

The International Journal of Developmental Biology ◽

10.1387/ijdb.200194rn ◽

2020 ◽

Vol 52 ◽

Cited By ~ 1

Author(s):

Alan Anuart González-Rangel ◽

Rosa E. Navarro

Keyword(s):

Oxidative Stress ◽

Stress Response ◽

Model Organism ◽

Cellular Functions ◽

C Elegans ◽

Stress Genes ◽

Larval Stages ◽

Pocket Protein ◽

And Oxidative Stress

The pocket protein family controls several cellular functions such as cell cycle, differentiation, and apoptosis, among others; however, its role in stress has been poorly explored. The roundworm Caenorhabditis elegans is a simple model organism whose genes are highly conserved during evolution. C. elegans has only one pocket protein, LIN-35; a pRB-related protein similar to p130. To control the expression of some of its targets, LIN-35 interacts with E2F-DP transcription factors and LIN-52, a member of SynMUV (Synthetic Muv complex). Together, these proteins form the DRM complex, which is also known as the DREAM complex in mammals. In this review, we will focus on the role of LIN-35 and its partners in the stress response. It has been shown that LIN-35 is required to control starvation in L1 and L4 larval stages, and to induce starvation-induced germ apoptosis. Remarkably, during L1 starvation, insulin/IGF-1 receptor signaling (IIS), as well as the pathogenic, toxin, and oxidative stress-responsive genes, are repressed by LIN-35. The lack of lin-35 also triggers a downregulation of oxidative stress genes. Recent works showed that lin-35 and hpl-2 mutant animals showed enhanced resistance to UPRER. Additionally, hpl-2 mutant animals also exhibited the upregulation of autophagic genes, suggesting that the SynMuv/DRM proteins participate in this process. Finally, lin-35(n745) mutant animals overexpressed hsp-6, a chaperone that participated in the UPRmt. All of these data demonstrate that LIN-35 and its partners play an important role during the stress response.

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