201: The role of candidate oxidative stress genes in the developmental programming of adult disease

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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Impact of Oxidative Stress in Fetal Programming

Journal of Pregnancy ◽

10.1155/2012/582748 ◽

2012 ◽

Vol 2012 ◽

pp. 1-8 ◽

Cited By ~ 124

Author(s):

Loren P. Thompson ◽

Yazan Al-Hasan

Keyword(s):

Oxidative Stress ◽

Organ Dysfunction ◽

Fetal Programming ◽

Target Genes ◽

Therapeutic Strategies ◽

Epigenetic Mechanisms ◽

Adult Disease ◽

Specific Target ◽

Increased Risk

Intrauterine stress induces increased risk of adult disease through fetal programming mechanisms. Oxidative stress can be generated by several conditions, such as, prenatal hypoxia, maternal under- and overnutrition, and excessive glucocorticoid exposure. The role of oxidant molecules as signaling factors in fetal programming via epigenetic mechanisms is discussed. By linking oxidative stress with dysregulation of specific target genes, we may be able to develop therapeutic strategies that protect against organ dysfunction in the programmed offspring.

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

Medical Science Monitor ◽

10.12659/msm.934161 ◽

2021 ◽

Vol 27 ◽

Author(s):

Di Lu ◽

Ning Yang ◽

Shuai Wang ◽

Wenyu Liu ◽

Di Zhang ◽

...

Keyword(s):

Oxidative Stress ◽

Stress Genes ◽

Predictive Role

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Abstract 311: Early Losartan Treatment Prevents the Developmental Programming of Cardiac Dysfunction Caused by Neonatal High Oxygen Exposure in Rats

Hypertension ◽

10.1161/hyp.64.suppl_1.311 ◽

2014 ◽

Vol 64 (suppl_1) ◽

Author(s):

Mariane Bertagnolli ◽

Sarah Béland-Bonenfant ◽

Anne Dios ◽

Daniela R Dartora ◽

Marie-Amélie Lukaszewski ◽

...

Keyword(s):

Oxidative Stress ◽

Cardiac Dysfunction ◽

Systolic Function ◽

Developmental Programming ◽

Term Treatment ◽

Short Term ◽

Short Term Treatment ◽

High O2 ◽

Cardiac Alterations

Neonatal oxidative stress is a major postnatal deleterious factor predisposing preterm born infants to classical complications of prematurity (retinopathy, bronchopulmonary dysplasia) which are characterized by impaired vascular development. Our group has previously shown that rats transiently exposed to high O2 as newborns (mimicking human preterms oxidative stress conditions) develop high blood pressure (BP), cardiac remodeling and dysfunction later in life, in part mediated by the renin angiotensin system (RAS). Cardiac RAS activation is characterized by AT1/AT2 receptors imbalance, with increased AT1R at adult age. In order to study the role of RAS at early stages of the developmental programming of cardiac dysfunction caused by high O2 exposure, we assessed whether an early and short-term treatment with AT1R blocker Losartan, prevents cardiac alterations at young male 4 wks-old rats (prior to the elevation of BP in this model). Sprague-Dawley newborns rats were kept with their mother in 80% O2 (O2 group, n=9) or room air (Ctrl, n=9) from days 3-10 of life (P3-P10). Losartan (LOS, n=10, 20 mg/Kg) or water was administered by gavage in O2 rats from P8-P10 (last 2 days of O2 to avoid impact on nephrogenesis). At 4 wks, echocardiography reveals that O2 rats have decreased fraction of shortening compared to Ctrl (FS: 37±2 vs 42±2 %), suggesting impaired systolic function in O2. Cardiac hypertrophy evaluated by heart/body weight and cardiomyocyte surface area (CSA) is also increased in O2 vs Ctrl (141±13 vs 118±4 μm2). LOS treatment prevented the impairment of systolic function in O2 by ameliorating FS (43±2 %) and reducing CSA (121±11 μm2). LOS treatment also modulated RAS genes expression (RT-PCR): LOS restored AT1/AT2 balance in O2 hearts by decreasing AT1b subunit (0.8±0.2 O2 vs 1.3±0.3 O2+LOS vs 0.9±0.2 Ctrl) as well as increasing ACE2 (1.5±0.4 O2 vs 0.8±0.1 O2+LOS vs 1.1±0.4 Ctrl) expressions. In conclusion, a short-term treatment with LOS during neonatal O2 exposure prevents the impairment of cardiac systolic function and hypertrophy at young age. This data reinforces the key role of RAS in the developmental programming of cardiac dysfunction and reveals LOS as an effective strategy to prevent early cardiac alterations caused by neonatal high O2 exposure.

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Abstract 135: Obesity Accelerates the Deterioration of Renal Function in Developmental Programming of Hypertension. Role of Angiotensin Ii and Oxidative Stress

Hypertension ◽

10.1161/hyp.68.suppl_1.135 ◽

2016 ◽

Vol 68 (suppl_1) ◽

Author(s):

Antonio Tapia ◽

Juan M Moreno ◽

Maria T Llinas ◽

F. Javier Salazar

Keyword(s):

Oxidative Stress ◽

Renal Function ◽

Angiotensin Ii ◽

Perinatal Period ◽

Developmental Programming ◽

Ang Ii ◽

Obese Rats ◽

Renal Vascular ◽

And Oxidative Stress

Numerous studies have shown gender-dependent differences in the deterioration of renal function in models of developmental programming of hypertension (DPH). It is also known that obesity is associated to changes in renal function and that both angiotensin II (Ang II) and oxidative stress are involved in the renal alterations that occur in obesity and in animals with DPH. The main objectives were to examine whether the increment of arterial pressure (AP) and the deterioration of renal function are accelerated as a consequence of obesity in SD rats with DPH; whether these changes are gender-dependent; and to evaluate the role of Ang II and oxidative stress in these AP and renal function changes. A high fat diet (60%) was given during the first 4 months of age and DPH was induced by an AT receptor antagonist during nephrogenic period (ARAnp). Systolic AP (mmHg) was greater (P<0.05) in ARAnp-obese rats (167 ± 3 in ♂; 146 ± 4 in ♀) than in ARAnp (155 ± 3 in ♂; 137 ± 3 in ♀); obese (147 ± 2 in ♂; 137 ± 2 in ♀) or control (127 ± 1 in ♂; 119 ± 2 in ♀) rats. Three days administration of candesartan (7 mg/kg/day) led to a decrease in AP that was greater (P<0.05) in ARAnp-obese rats (55 ± 3 in ♂; 45 ± 4 in ♀) than in ARAnp (40 ± 3 in ♂; 37 ± 4 in ♀); obese (38 ± 4 in ♂; 27 ± 4 in ♀) or control (12 ± 2 in ♂; 14 ± 3 in ♀) rats. The acute Ang II infusion (30 ng/kg/min) induced an increase in renal vascular resistance (mmHg/ml/min/gr kw) that was also greater in ARAnp-obese rats (217 ± 45% in ♂; 145 ± 38% in ♀) than in ARAnp (103 ± 9% in ♂; 97 ± 8% in ♀); obese (106 ± 14% in ♂; 106 ± 17 in ♀) or control (51 ± 7% in ♂; 51 ± 10% in ♀) rats. The response to candesartan or Ang II infusion in ARAnp-obese rats was gender-dependent and may be explained by an enhanced oxidative stress. The expression of P67phox in the renal cortex was greater (P<0.05) in ARAnp-obese rats (3,00 ± 0,05 in ♂; 2,60 ± 0,04 in ♀) than in ARAnp (1,16 ± 0,04 in ♂; 1,66 ± 0,03 in ♀); obese (0,94 ± 0,06 in ♂; 1,02 ± 0,02 in ♀) or control (1,00 ± 0,02 in ♂; 1,02 ± 0,023 in ♀) rats. The results of this study suggest that obesity at an early age enhances the hypertension and accelerates the deterioration of renal function that occurs when cardiovascular disease is programmed during the perinatal period. It is also shown that Ang II and oxidative stress seems to play an important role in these AP and renal function changes.

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