scholarly journals DNA Damage and Neutrophil Elastase in Children with Prader-Willi Syndrome

2019 ◽  
Vol 12 (04) ◽  
pp. 1967-1974
Author(s):  
Moushira Erfan Zaki ◽  
Eman Youness ◽  
Mohamed Gadelhak ◽  
Marwa Shehab ◽  
Safinaz El-Toukhy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Neutrophil Elastase ◽  
Fat Body ◽  
Inflammatory Marker ◽  
The Body ◽  
Low Grade ◽  
Prader Willi Syndrome ◽  
Antioxidant Mechanism ◽  
Leukocyte Dna Damage

Obesity is the most common cause of metabolic problems in Prader-Willi syndrome (PWS). Obesity has been joined to a low grade pro-inflammatory state, in which impairments in the oxidative stress and antioxidant mechanism could be involved. The aim of the work is to investigate the level of DNA damage and inflammatory marker neutrophil elastase in PWS patients. The study included 21 children with PWS detected by fluorescence in situ hybridization (FISH) method and 20 age and sex healthy matched obese controls. Their mean age was 6 ± 2.24 years. Leukocyte DNA damage was evaluated by comet assay and neutrophil elastase was assessed by ELISA. All patients presented with distinctive faces, hypotonia, obesity, short stature and various other criteria. FISH revealed deletion 15q11–13 in all PWS patients. The mean of DNA damage frequency was significantly higher in PWS than controls. The body fat%, body mass index (BMI) z score were elevated in PWS cases. Moreover, the neutrophil elastase was significantly higher in patients compared to controls. The present study highlights the existence of oxidative stress and inflammation in Prader Willi syndrome that may have a role in the management and treatment of these patients.

scholarly journals Oxidative Stress, Neutrophil Elastase and Vascular Endothelial Growth Factor in Obese Pregnant Women with Preeclampsia

2019 ◽  
Vol 12 (04) ◽  
pp. 1887-1891
Author(s):  
Moushira Zakia ◽  
Taghreed Shalabi ◽  
Tamer Hussein ◽  
Mohamed Hammam ◽  
Eman Youness ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Blood Pressure ◽  
Growth Factor ◽  
Pregnant Women ◽  
Neutrophil Elastase ◽  
Inflammatory Marker ◽  
Vascular Endothelial ◽  
Obese Women ◽  
Endothelial Growth Factor

Oxidative stress, inflammation, and vascular endothelial proliferation and obesity are risk factors associated with preeclampsia (PE). Thepresent study aimed to investigate the levels of malondialdehyde (MDA) as a putative circulatory marker of oxidative stress, neutrophil Elastase (NE) as inflammatory marker andvascular endothelial growth factor (VEGF) as marker for vascular permeability-enhancing activities inobese women withpreeclampsia PE and compare withnormal pregnancy women. The study was carried out on 50 pregnant obese women with PE and 50 normal pregnant women. The preeclampsia women were characterized with high blood pressure 160/110 mmHg and proteinuria. The gestational age ranged from ≥32 weeks to <37 weeks. Pre pregnancyweightwas recorded. Body mass index (BMI) was calculatedat delivery.SerumMDA, NEand VEGF were estimatedby ELISA. Significant higher levels of serum MAD,NE and VEGF were observed in obese PE patients as compared to normal controls. Our results suggested thatobesity;oxidative stress, NEandVEGFbiomarkers are risk factors for PE,emphasizing their role as feasible candidate risk markersfor cases withhigh blood pressure in early pregnancy.

The Effects of Polymer Coating of Gold Nanoparticles on Oxidative Stress and DNA Damage

2020 ◽  
Vol 39 (4) ◽  
pp. 328-340
Author(s):  
Gamze Tilbe Sen ◽  
Gizem Ozkemahli ◽  
Reza Shahbazi ◽  
Pınar Erkekoglu ◽  
Kezban Ulubayram ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Weight ◽  
Dna Damage ◽  
Gold Nanoparticles ◽  
Polyethylene Glycol ◽  
High Molecular Weight ◽  
Hepg2 Cells ◽  
The Body ◽  
Low Molecular Weight ◽  
Antioxidant Parameters

Gold nanoparticles (AuNPs) have been widely used in many biological and biomedical applications. In this regard, their surface modification is of paramount importance in order to increase their cellular uptake, delivery capability, and optimize their distribution inside the body. The aim of this study was to examine the effects of AuNPs on cytotoxicity, oxidant/antioxidant parameters, and DNA damage in HepG2 cells and investigate the potential toxic effects of different surface modifications such as polyethylene glycol (PEG) and polyethyleneimine (PEI; molecular weights of 2,000 (low molecular weight [LMW]) and 25,000 (high molecular weight [HMW]). The study groups were determined as AuNPs, PEG-coated AuNPs (AuNPs/PEG), low-molecular weight polyethyleneimine-coated gold nanoparticles (AuNPs/PEI LMW), and high-molecular weight polyethyleneimine-coated gold nanoparticles (AuNPs/PEI HMW). After incubating HepG2 cells with different concentrations of nanoparticles for 24 hours, half maximal inhibitory concentrations (the concentration that kills 50% of the cells) were determined as 166.77, 257.73, and 198.44 µg/mL for AuNPs, AuNPs/PEG, and AuNPs/PEI LMW groups, respectively. Later, inhibitory concentration 30 (IC30, the concentration that kills 30% of the cells) doses were calculated, and further experiments were performed on cells that were exposed to IC30 doses. Although intracellular reactive oxygen species levels significantly increased in all nanoparticles, AuNPs as well as AuNPs/PEG did not cause any changes in oxidant/antioxidant parameters. However, AuNPs/PEI HMW particularly induced oxidative stress as evidence of alterations in lipid peroxidation and protein oxidation. These results suggest that at IC30 doses, AuNPs do not affect oxidative stress and DNA damage significantly. Polyethylene glycol coating does not have an impact on toxicity, however PEI coating (particularly HMW) can induce oxidative stress.

scholarly journals Ultraviolet Radiation-Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Uraiwan Panich ◽  
Gunya Sittithumcharee ◽  
Natwarath Rathviboon ◽  
Siwanon Jirawatnotai
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Dna Damage ◽  
Mesenchymal Stem Cells ◽  
Stem Cell ◽  
Ultraviolet Radiation ◽  
Skin Aging ◽  
The Body ◽  
And Oxidative Stress

Skin is the largest human organ. Skin continually reconstructs itself to ensure its viability, integrity, and ability to provide protection for the body. Some areas of skin are continuously exposed to a variety of environmental stressors that can inflict direct and indirect damage to skin cell DNA. Skin homeostasis is maintained by mesenchymal stem cells in inner layer dermis and epidermal stem cells (ESCs) in the outer layer epidermis. Reduction of skin stem cell number and function has been linked to impaired skin homeostasis (e.g., skin premature aging and skin cancers). Skin stem cells, with self-renewal capability and multipotency, are frequently affected by environment. Ultraviolet radiation (UVR), a major cause of stem cell DNA damage, can contribute to depletion of stem cells (ESCs and mesenchymal stem cells) and damage of stem cell niche, eventually leading to photoinduced skin aging. In this review, we discuss the role of UV-induced DNA damage and oxidative stress in the skin stem cell aging in order to gain insights into the pathogenesis and develop a way to reduce photoaging of skin cells.

scholarly journals Association of Anthropometric Measurements With Oxidant-Antioxidant Status Among Young Saudi Females

2018 ◽  
pp. 787-793
Author(s):  
R. LATIF ◽  
N. RAFIQUE
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Body Fat ◽  
Positive Association ◽  
Normal Weight ◽  
The Body ◽  
Anthropometric Measurements ◽  
Oxidative Stress Biomarkers ◽  
Obese Adolescent ◽  
Stress Biomarkers

Present study aimed to explore the levels and correlation of oxidative stress biomarkers with anthropometry in a population of young Saudi females. One hundred six normotensives, non-diabetic Saudi females, with minimally active lifestyle, based on their body mass index (BMI) were divided as; normal-weight (NW; n=52), overweight (OW; n=24) and obese (OB; n=30). Anthropometric measurements [BMI, Waist Circumference (WC), Waist-Hip Ratio (WHR), Body Density (BD), Body Adiposity Index (BAI), % Body fat] and oxidative stress biomarkers; Thiobarbituric acid reactive substances (TBARS), 8-hydroxy-2-deoxyguanosine (8-OH-2dG: indicative of DNA/RNA damage), Superoxide dismutase, Serum total antioxidant capacity) were recorded. There was statistically significant higher 8-OH-2dG (pg/ml) in OB compared to NW (800.63±6.19 vs. 780.22±3.34; p=0.007), as determined by one-way ANOVA and Tukey post hoc test. 8-OH-2dG was significantly and positively associated with BMI (r=0.286, p=0.004), WC (r=0.280, p=0.005), BAI (r=0.26, p=0.008), and % body fat (r=0.27, p=0.006). There may be significantly increased DNA damage in normoglycemic, normotensive obese adolescent females. This can be linked to the amount of adipose tissue in the body as depicted by strong positive association between DNA damage and BMI, WC, BAI, and % body fat.

Overloaded Training Increases Exercise-Induced Oxidative Stress and Damage

2003 ◽  
Vol 28 (4) ◽  
pp. 588-604 ◽  
Author(s):  
Stephane Palazzetti ◽  
Marie-Jeanne Richard ◽  
Alain Favier ◽  
Irene Margaritis
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Defense Mechanism ◽  
Induced Response ◽  
Tbars Level ◽  
Sod Activity ◽  
Activity Increase ◽  
Before And After ◽  
Exercise Induced ◽  
Leukocyte Dna Damage

We hypothesized that overloaded training (OT) in triathlon would induce oxidative stress and damage on muscle and DNA. Nine male triathletes and 6 male sedentary subjects participated in this study. Before and after a 4-week OT, triathletes exercised for a duathlon. Blood ratio of reduced vs. oxidized glutathione (GSH/GSSG), plasma thiobarbituric acid reactive substances (TEARS), leukocyte DNA damage, creatine kinase (CK), and CK-MB mass in plasma, erythrocyte superoxide dismutase (SOD) activity, erythrocyte and plasma glutathione peroxidase (GSH-Px) activities, and plasma total antioxidant status (TAS) were measured before and after OT in pre- and postexercise situations. Triathletes were overloaded in response to OT. In rest conditions, OT induced plasma GSH-Px activity increase and plasma TAS decrease (both p < 0.05). In exercise conditions, OT resulted in higher exercise-induced variations of blood GSH/GSSG ratio, TBARS level (both p < 0.05), and CK-MB mass (p < 0.01) in plasma; and decreased TAS response (p < 0.05). OT could compromise the antioxidant defense mechanism with respect to exercise-induced response. The resulting increased exercise-induced oxidative stress and further cellular susceptibility to damage needs more study. Key words: lipid peroxidation, leukocyte DNA damage, antioxidant, triathlon

scholarly journals Oxidative stress, cholinesterase activity, and DNA damage in the liver, whole blood, and plasma of Wistar rats following a 28-day exposure to glyphosate

2018 ◽  
Vol 69 (2) ◽  
pp. 154-168 ◽  
Author(s):  
Mirta Milić ◽  
Suzana Žunec ◽  
Vedran Micek ◽  
Vilena Kašuba ◽  
Anja Mikolić ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Wistar Rats ◽  
Cholinesterase Activity ◽  
Daily Intake ◽  
The Body ◽  
Control Treatment ◽  
Exposure Level ◽  
Tbars Level ◽  
Significant Drop

AbstractIn this 28 day-study, we evaluated the effects of herbicide glyphosate administered by gavage to Wistar rats at daily doses equivalent to 0.1 of the acceptable operator exposure level (AOEL), 0.5 of the consumer acceptable daily intake (ADI), 1.75 (corresponding to the chronic population-adjusted dose, cPAD), and 10 mg kg−1 body weight (bw) (corresponding to 100 times the AOEL). At the end of each treatment, the body and liver weights were measured and compared with their baseline values. DNA damage in leukocytes and liver tissue was estimated with the alkaline comet assay. Oxidative stress was evaluated using a battery of endpoints to establish lipid peroxidation via thiobarbituric reactive substances (TBARS) level, level of reactive oxygen species (ROS), glutathione (GSH) level, and the activity of glutathione peroxidase (GSH-Px). Total cholinesterase activity and the activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) were also measured. The exposed animals gained less weight than control. Treatment resulted in significantly higher primary DNA damage in the liver cells and leukocytes. Glyphosate exposure significantly lowered TBARS in the liver of the AOEL, ADI, and cPAD groups, and in plasma in the AOEL and cPAD group. AChE was inhibited with all treatments, but the AOEL and ADI groups significantly differed from control. Total ChE and plasma/liver ROS/GSH levels did not significantly differ from control, except for the 35 % decrease in ChE in the AOEL and ADI groups and a significant drop in liver GSH in the cPAD and 100xAOEL groups. AOEL and ADI blood GSH-Px activity dropped significantly, but in the liver it significantly increased in the ADI, cPAD, and 100xAOEL groups vs. control. All these findings show that even exposure to low glyphosate levels can have serious adverse effects and points to a need to change the approach to risk assessment of low-level chronic/sub-chronic glyphosate exposure, where oxidative stress is not necessarily related to the genetic damage and AChE inhibition.

scholarly journals Measurement of Serum Chemerin, Oxidized LDL, and Vitamin D Levels in Prader–Willi Syndrome: A Cross-Sectional Study in Pediatric Egyptian Patients

2020 ◽  
Vol 10 (01) ◽  
pp. e187-e195
Author(s):  
Manal M. Thomas ◽  
Moushira E. Zaki ◽  
Eman Youness ◽  
Khaled Hamed ◽  
Azzah A. Khedr ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Research Centre ◽  
Enzyme Linked Immunosorbent Assay ◽  
Low Grade ◽  
Prader Willi Syndrome ◽  
Healthy Children ◽  
Vitamin D Levels ◽  
Egyptian Patients ◽  
Low Grade Inflammation

AbstractPrader–Willi syndrome (PWS) is the commonest genetic cause of obesity. Oxidative stress and chronic low-grade inflammation play a crucial role in the pathogenesis of obesity. Alterations of vitamin D (25-OHD) levels are commonly encountered with obesity. The aim of this study was to analyze serum chemerin, oxidized low-density lipoprotein (ox-LDL), and 25-OHD values in pediatric PWS patients in comparison with obese healthy children and nonobese control groups, highlighting possible correlations with body mass index (BMI) and obesity. Twenty-six PWS Egyptian patients and 26 obese healthy individuals referred to the outpatient clinic of the Clinical Genetics Department, National Research Centre, Cairo, Egypt, and 20 control patients with matching age and sex were enrolled in the study. Patients were clinically diagnosed and confirmed by routine cytogenetic and fluorescence in-situ hybridization analysis. Anthropometric measurements were performed, and BMI was calculated by weight/height2 (kg/m2), and BMI z score was also determined. Serum chemerin, ox-LDL, and vitamin D were determined by enzyme-linked immunosorbent assay. Chemerin levels, which reflected chronic inflammation, were significantly elevated as compared with obese and nonobese controls (p ≤ 0.0001). Concerning oxidative damage, children with PWS showed higher Ox-LDL levels compared with obese and nonobese controls (p < 0.0001). Vitamin D levels were significantly lower in PWS patients compared with obese and nonobese controls (p ≤ 0.0001). Our data showed that obesity in PWS is associated with oxidative stress and chronic low-grade inflammation. Ox-LDL is a good indicator of oxidative stress, and chemerin could be used as a biomarker for the chronic inflammatory state. Furthermore, vitamin D supplementation is recommended in PWS patients

scholarly journals Cardiac Inflammation, Oxidative Stress, Nrf2 Expression, and Coagulation Events in Mice with Experimental Chronic Kidney Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Abderrahim Nemmar ◽  
Suhail Al-Salam ◽  
Sumaya Beegam ◽  
Nur Elena Zaaba ◽  
Javed Yasin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Dna Damage ◽  
Kidney Disease ◽  
Troponin I ◽  
The Body ◽  
Control Group ◽  
Cardiac Inflammation ◽  
Nrf2 Expression

Chronic kidney disease (CKD) is known to be associated with cardiovascular dysfunction. Dietary adenine intake in mice is also known to induce CKD. However, in this experimental model, the mechanisms underlying the cardiotoxicity and coagulation disturbances are not fully understood. Here, we evaluated cardiac inflammation, oxidative stress, DNA damage, and coagulation events in mice with adenine (0.2% w / w in feed for 4 weeks)-induced CKD. Control mice were fed with normal chow for the same duration. Adenine increased water intake, urine output, relative kidney weight, the plasma concentrations of urea and creatinine, and the urinary concentrations of kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin. It also decreased the body weight and creatinine clearance, and caused kidney DNA damage. Renal histological analysis showed tubular dilation and damage and neutrophilic influx. Adenine induced a significant increase in systolic blood pressure and the concentrations of troponin I, tumor necrosis factor-α, and interleukin-1β in heart homogenates. It also augmented the levels of markers of lipid peroxidation measured by malondialdehyde production and 8-isoprostane, as well as the antioxidants superoxide dismutase and catalase. Immunohistochemical analysis of the hearts showed that adenine increased the expression of nuclear factor erythroid-derived 2-like 2 by cardiomyocytes. It also caused cardiac DNA damage. Moreover, compared with the control group, adenine induced a significant increase in the number of circulating platelet and shortened the thrombotic occlusion time in pial arterioles and venules in vivo, and induced a significant reduction in the prothrombin time and activated partial thromboplastin time. In conclusion, the administration of adenine in mice induced CKD-associated cardiac inflammation, oxidative stress, Nrf2 expression, and DNA damage. It also induced prothrombotic events in vivo. Therefore, this model can be satisfactorily used to study the cardiac pathophysiological events in subjects with CKD and the effect of drug treatment thereon.

scholarly journals STUDI PRELIMINARI TENTANG PENGARUH D-GALAKTOSA DALAM MENGINDUKSI STRES OKSIDATIF PADA MENCIT JANTAN GALUR OUTBRED FK USU

2019 ◽  
Vol 2 (1) ◽  
pp. 1-5
Author(s):  
Siti Sarah Bintang Sarah Bintang ◽  
Yahwardiah Siregar ◽  
Muhammad Ichwan
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Dna Damage ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
The Body ◽  
Blood Collection ◽  
Male Mice ◽  
North Sumatra

Abstract Oxidative stress occurs due to imbalance of free radicals over antioxidant level in the body. This condition causes lipid peroxidation and DNA damage. D-Galaktosa is The mechanism of oxidative stress induced by d-galactose occurs in the subcellular, especially in the brain's mitochondria. Increasing the concentration of d-galaktosa is oxidized by galaktosa oxidase to form hydrogen peroxide (H202) which causes a decrease in superoxide dismutase (SOD). H202 reacts with reduced iron and forms hydroxide ions (OH-). Objective: The aim of this study was to determine the effect of d-galaktosa induction on oxidative stress levels (MDA) in male mice. Methods: Methods of samples of mice given d-galaktosa and blood collection from the heart were carried out at the Pharmacology Laboratory of the Faculty of Medicine, University of North Sumatra. Results: The results showed that administration of d-galaktosa, through intraperitonial injection every day for 6 weeks, had an effect on the levels of oxidative stress in male mice. Conclusion: The results of this study indicate that administration of d-galaktosa, through intraperitonial injection every day for 6 weeks, has an effect on levels of oxidative stress in male mice.

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