scholarly journals Associations between Levels of Urinary Oxidative Stress of 8-OHdG and Risk of Atopic Diseases in Children

2020 ◽  
Vol 17 (21) ◽  
pp. 8207
Author(s):  
Pang-Yen Chen ◽  
Chien-Wei Chen ◽  
Yu-Jang Su ◽  
Wen-Han Chang ◽  
Wei-Fong Kao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Large Scale ◽  
Reference Group ◽  
Allergic Diseases ◽  
Kindergarten Children ◽  
Sample Survey ◽  
Atopic Diseases ◽  
Childhood Environment ◽  
Underlying Mechanisms ◽  
Oxidative Products

The oxidative stress biomarker of urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) was reported to be changed in patients with allergic diseases. Measurement of urinary oxidative products is noninvasive. However, correlations between the severity levels of atopic diseases and oxidative stress remain unclear. This study aimed to investigate the association among urinary 8-OHdG, atopic dermatitis (AD), and the phenotypes of atopic diseases in children. In a nested case-control study, participants of kindergarten children were enrolled from the Childhood Environment and Allergic Diseases Study (CEAS). Urinary analyses and urinary 8-OHdG were performed on samples from 200 children with AD as cases and 200 age- and sex-matched controls. Our study presents the following main findings: (1) The urinary 8-OHdG levels were significantly higher in cases than controls. Higher urinary 8-OHdG levels were associated with the risk of AD in a dose-response-manner; (2) Children’s AD history was associated with higher risks of asthma, allergic rhinitis, and night pruritus; (3) For children with AD, urinary 8-OHdG levels of >75th percentile were associated with higher risk of asthma, compared with the reference group of 0–25th percentiles. In summary, this study provides better understanding of the underlying mechanisms of AD and urinary 8-OHdG by analyzing a large-scale sample survey in Taiwan.

scholarly journals “Cumulative Stress”: The Effects of Maternal and Neonatal Oxidative Stress and Oxidative Stress-Inducible Genes on Programming of Atopy

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Sara Manti ◽  
Lucia Marseglia ◽  
Gabriella D’Angelo ◽  
Caterina Cuppari ◽  
Erika Cusumano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Sequences ◽  
Allergic Diseases ◽  
Atopic Diseases ◽  
Cumulative Stress ◽  
Inducible Genes ◽  
The Relationship ◽  
And Oxidative Stress ◽  
Epigenetic Pattern

Although extensive epidemiological and laboratory studies have been performed to identify the environmental and immunological causes of atopy, genetic predisposition seems to be the biggest risk factor for allergic diseases. The onset of atopic diseases may be the result of heritable changes of gene expression, without any alteration in DNA sequences occurring in response to early environmental stimuli. Findings suggest that the establishment of a peculiar epigenetic pattern may also be generated by oxidative stress (OS) and perpetuated by the activation of OS-related genes. Analyzing the role of maternal and neonatal oxidative stress and oxidative stress-inducible genes, the purpose of this review was to summarize what is known about the relationship between maternal and neonatal OS-related genes and the development of atopic diseases.

Atopie als Vorbote von Autoimmunerkrankungen - Nicht aus dem (zweiten) Blick verlieren

2018 ◽  
Vol 6 (2) ◽  
pp. 85-86
Author(s):  
David Brandt
Keyword(s):  
Allergic Rhinitis ◽  
Large Scale ◽  
Past History ◽  
Systemic Vasculitis ◽  
Allergic Diseases ◽  
Control Group ◽  
Atopic Diseases ◽  
Cross Sectional ◽  
Large Scale Study ◽  
History Of

Background: Kawasaki disease (KD) is an acute, systemic vasculitis in children, with an etiology that is not completely understood. It is assumed that the development of KD is mediated by an immunologic response. Several reports from East Asia have found a higher prevalence of atopic diseases among patients with KD, but a large-scale study of a non-Asian population regarding this correlation is still lacking. The purpose of this article was to achieve this goal. Methods: We conducted a cross-sectional, large-scale study to estimate the correlation of KD with allergic diseases. The medical history of 1,187,757 Israeli teenagers (aged 16-20 years during the years 1998-2013) was retrieved. The study population was divided into 3 groups according to a past history of noncomplicated and complicated KD and a control group. The prevalence of allergic diseases among these groups was further investigated. Results: The prevalence of atopic diseases in the 3 study groups was presented (asthma in 11.4, 8.1 and 3.5%, respectively; angioedema/urticaria in 7.1, 0 and 0.46%, respectively; allergic rhinitis in 20, 12.1 and 6.7%, respectively). In noncomplicated KD, a statistically significant link to asthma [odds ratio (OR) 2.4; p = 0.048] and a borderline significant link to allergic rhinitis (OR 1.9; p = 0.06) were found. In KD complicated with cardiac disease, statistically significant links were found for all the allergic conditions, asthma (OR 3.5; p = 0.003), allergic rhinitis (OR 3.5; p < 0.001) and angioedema/urticaria (OR 16.48; p < 0.001). Conclusion: KD is associated with allergic diseases. This association increases with the severity of the disease.

Iron Metabolism in the Human Body and Setting its Hygienic Limits for Drinking Water. Review. Part 2

2020 ◽  
Vol 99 (5) ◽  
pp. 504-508
Author(s):  
Natalija A. Egorova ◽  
N. V. Kanatnikova
Keyword(s):  
Oxidative Stress ◽  
Drinking Water ◽  
Iron Overload ◽  
Iron Metabolism ◽  
Subcutaneous Tissue ◽  
Allergic Diseases ◽  
The Body ◽  
Urogenital System ◽  
High Iron Content ◽  
Labile Iron Pool

Iron is an assential element for the growth, division, differentiation and functioning of any cell in the body. Iron is virtually important for human and danger at the same time, because with excessive accumulation it causes oxidative stress with formation of highly active oxygen radicals and reactive form of nitrogen that can destroy cell membranes, proteins, nucleic acids, reduce cell viability, with, according to modern concepts, can contribute to the development of many diseases (cardiovascular, rheumatic, gastrointestinal, neurodegenerative, oncological, metabolic and others), and also accelerate the aging process. Part 1 of this review discussed the issues of iron metabolism in human, including its regulation at the cellular and systemic levels, the intake, transport, use, accumulation and export of iron in cells, the role of the labile iron pool in the cytoplasm of cells and plasma non-transferrin bound iron. Data are provided on the causes, frequency and significance of iron overload in the formation of free radicals and the development of oxidative stress. Part 2 of the review provides information on diseases associated with iron overload as well as information on ferroptosis - a new type of iron-dependent regulated cell death. Attention is paid to the works of domestic authors, where it was found that prolonged use of drinking water with a high iron content is unfavorable for the population and leads to an increase in the overall incidence, the development of the diseases of the blood, skin and subcutaneous tissue, musculoskeletal system, digestive system, urogenital system, and allergic diseases. Separate publications are cited on the possibility of a negative effect of iron at concentrations in water of 0.3 mg/l and lower. The material of the review emphasizes the preventive significance of caution attitude to regulating iron in the water in the Russian Federation, where 1/3 of the population uses iron-containing water for drinking, and substantiate the feasibility of establishing a hygienic limit for iron in water not higher than 0.3 mg/l.

Evolution of Metastable Structures in Bimetallic Catalysts from Microscopy and Machine-Learning Molecular Dynamics

2020 ◽  
Author(s):  
Jin Soo Lim ◽  
Jonathan Vandermause ◽  
Matthijs A. van Spronsen ◽  
Albert Musaelian ◽  
Christopher R. O’Connor ◽  
...  
Keyword(s):  
Machine Learning ◽  
Molecular Dynamics ◽  
Large Scale ◽  
Materials Science ◽  
Complete Characterization ◽  
Layer By Layer ◽  
Surface Restructuring ◽  
Metastable Structures ◽  
Mechanistic Investigation ◽  
Underlying Mechanisms

Restructuring of interface plays a crucial role in materials science and heterogeneous catalysis. Bimetallic systems, in particular, often adopt very different composition and morphology at surfaces compared to the bulk. For the first time, we reveal a detailed atomistic picture of the long-timescale restructuring of Pd deposited on Ag, using microscopy, spectroscopy, and novel simulation methods. Encapsulation of Pd by Ag always precedes layer-by-layer dissolution of Pd, resulting in significant Ag migration out of the surface and extensive vacancy pits. These metastable structures are of vital catalytic importance, as Ag-encapsulated Pd remains much more accessible to reactants than bulk-dissolved Pd. The underlying mechanisms are uncovered by performing fast and large-scale machine-learning molecular dynamics, followed by our newly developed method for complete characterization of atomic surface restructuring events. Our approach is broadly applicable to other multimetallic systems of interest and enables the previously impractical mechanistic investigation of restructuring dynamics.

Inflammatory Biomarkers in Atrial Fibrillation

2019 ◽  
Vol 26 (5) ◽  
pp. 837-854 ◽  
Author(s):  
Effimia Zacharia ◽  
Nikolaos Papageorgiou ◽  
Adam Ioannou ◽  
Gerasimos Siasos ◽  
Spyridon Papaioannou ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Plasma Levels ◽  
Large Scale ◽  
Inflammatory Biomarkers ◽  
Inflammatory Pathways ◽  
Inflammatory State ◽  
Anti Inflammatory ◽  
Underlying Mechanisms

During the last few years, a significant number of studies have attempted to clarify the underlying mechanisms that lead to the presentation of atrial fibrillation (AF). Inflammation is a key component of the pathophysiological processes that lead to the development of AF; the amplification of inflammatory pathways triggers AF, and, in tandem, AF increases the inflammatory state. Indeed, the plasma levels of several inflammatory biomarkers are elevated in patients with AF. In addition, the levels of specific inflammatory biomarkers may provide information regarding to the AF duration. Several small studies have assessed the role of anti-inflammatory treatment in atrial fibrillation but the results have been contradictory. Large-scale studies are needed to evaluate the role of inflammation in AF and whether anti-inflammatory medications should be routinely administered to patients with AF.

Phytosomal Curcumin Elicits Anti-tumor Properties Through Suppression of Angiogenesis, Cell Proliferation and Induction of Oxidative Stress in Colorectal Cancer

2019 ◽  
Vol 24 (39) ◽  
pp. 4626-4638 ◽  
Author(s):  
Reyhaneh Moradi-Marjaneh ◽  
Seyed M. Hassanian ◽  
Farzad Rahmani ◽  
Seyed H. Aghaee-Bakhtiari ◽  
Amir Avan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Therapeutic Potential ◽  
Vegf Signaling ◽  
Anticancer Effects ◽  
Inhibition Of Angiogenesis ◽  
Underlying Mechanisms ◽  
Apoptotic Activity

Background: Colorectal cancer (CRC) is one of the most common causes of cancer-associated mortality in the world. Anti-tumor effect of curcumin has been shown in different cancers; however, the therapeutic potential of novel phytosomal curcumin, as well as the underlying molecular mechanism in CRC, has not yet been explored. Methods: The anti-proliferative, anti-migratory and apoptotic activity of phytosomal curcumin in CT26 cells was assessed by MTT assay, wound healing assay and Flow cytometry, respectively. Phytosomal curcumin was also tested for its in-vivo activity in a xenograft mouse model of CRC. In addition, oxidant/antioxidant activity was examined by DCFH-DA assay in vitro, measurement of malondialdehyde (MDA), Thiol and superoxidedismutase (SOD) and catalase (CAT) activity and also evaluation of expression levels of Nrf2 and GCLM by qRT-PCR in tumor tissues. In addition, the effect of phytosomal curcumin on angiogenesis was assessed by the measurement of VEGF-A and VEGFR-1 and VEGF signaling regulatory microRNAs (miRNAs) in tumor tissue. Results: Phytosomal curcumin exerts anti-proliferative, anti-migratory and apoptotic activity in-vitro. It also decreases tumor growth and augmented 5-fluorouracil (5-FU) anti-tumor effect in-vivo. In addition, our data showed that induction of oxidative stress and inhibition of angiogenesis through modulation of VEGF signaling regulatory miRNAs might be underlying mechanisms by which phytosomal curcumin exerted its antitumor effect. Conclusion: Our data confirmed this notion that phytosomal curcumin administrates anticancer effects and can be used as a complementary treatment in clinical settings.

Could Antioxidant Supplementation Delay Progression of Cardiovascular Disease in End-Stage Renal Disease Patients?

2020 ◽  
Vol 19 (1) ◽  
pp. 41-54 ◽  
Author(s):  
Stefanos Roumeliotis ◽  
Athanasios Roumeliotis ◽  
Xenia Gorny ◽  
Peter R. Mertens
Keyword(s):  
Oxidative Stress ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Close Association ◽  
Omega 3 ◽  
Endstage Renal Disease ◽  
Increased Risk ◽  
Underlying Mechanisms ◽  
Stage Renal Disease ◽  
End Stage

In end-stage renal disease patients, the leading causes of mortality are of cardiovascular (CV) origin. The underlying mechanisms are complex, given that sudden heart failure is more common than acute myocardial infarction. A contributing role of oxidative stress is postulated, which is increased even at early stages of chronic kidney disease, is gradually augmented in parallel to progression to endstage renal disease and is further accelerated by renal replacement therapy. Oxidative stress ensues when there is an imbalance between reactive pro-oxidants and physiologically occurring electron donating antioxidant defence systems. During the last decade, a close association of oxidative stress with accelerated atherosclerosis and increased risk for CV and all-cause mortality has been established. Lipid peroxidation has been identified as a trigger for endothelial dysfunction, the first step towards atherogenesis. In order to counteract the deleterious effects of free radicals and thereby ameliorate, or delay, CV disease, exogenous administration of antioxidants has been proposed. Here, we attempt to summarize existing data from studies that test antioxidants for CV protection, such as vitamins E and C, statins, omega-3 fatty acids and N-acetylcysteine.

Exercise and Stevia Rebaudiana (R) Extracts Attenuate Diabetic Cardiomyopathy in Type 2 Diabetic Rats: Possible Underlying Mechanisms

2020 ◽  
Vol 20 (7) ◽  
pp. 1117-1132
Author(s):  
Abdelaziz M. Hussein ◽  
Elsayed A. Eid ◽  
Ismaeel Bin-Jaliah ◽  
Medhat Taha ◽  
Lashin S. Lashin
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Diabetic Cardiomyopathy ◽  
Caspase 3 ◽  
Stevia Rebaudiana ◽  
Diabetic Rats ◽  
Control Group ◽  
Underlying Mechanisms ◽  
Type 2 Diabetic

Background and Aims: In the current work, we studied the effects of exercise and stevia rebaudiana (R) extracts on diabetic cardiomyopathy (DCM) in type 2 diabetic rats and their possible underlying mechanisms. Methods: : Thirty-two male Sprague Dawley rats were randomly allocated into 4 equal groups; a) normal control group, b) DM group, type 2 diabetic rats received 2 ml oral saline daily for 4 weeks, c) DM+ Exercise, type 2 diabetic rats were treated with exercise for 4 weeks and d) DM+ stevia R extracts: type 2 diabetic rats received methanolic stevia R extracts. By the end of the experiment, serum blood glucose, HOMA-IR, insulin and cardiac enzymes (LDH, CK-MB), cardiac histopathology, oxidative stress markers (MDA, GSH and CAT), myocardial fibrosis by Masson trichrome, the expression of p53, caspase-3, α-SMA and tyrosine hydroxylase (TH) by immunostaining in myocardial tissues were measured. Results: T2DM caused a significant increase in blood glucose, HOMA-IR index, serum CK-MB and LDH, myocardial damage and fibrosis, myocardial MDA, myocardial α-SMA, p53, caspase-3, Nrf2 and TH density with a significant decrease in serum insulin and myocardial GSH and CAT (p< 0.05). On the other hand, treatment with either exercise or stevia R extracts significantly improved all studied parameters (p< 0.05). Moreover, the effects of stevia R was more significant than exercise (p< 0.05). Conclusion: Both exercise and methanolic stevia R extracts showed cardioprotective effects against DCM and Stevia R offered more cardioprotective than exercise. This cardioprotective effect of these lines of treatment might be due to attenuation of oxidative stress, apoptosis, sympathetic nerve density and fibrosis and upregulation of the antioxidant transcription factor, Nrf2.

scholarly journals Blood–brain barrier disruption and ventricular enlargement are the earliest neuropathological changes in rats with repeated sub-concussive impacts over 2 weeks

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bailey Hiles-Murison ◽  
Andrew P. Lavender ◽  
Mark J. Hackett ◽  
Joshua J. Armstrong ◽  
Michael Nesbit ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Brain Barrier ◽  
Hippocampal Formation ◽  
Brain Barrier ◽  
Lateral Ventricles ◽  
Blood Brain Barrier Disruption ◽  
Blood Brain ◽  
Brain Barrier Disruption ◽  
Underlying Mechanisms

AbstractRepeated sub-concussive impact (e.g. soccer ball heading), a significantly lighter form of mild traumatic brain injury, is increasingly suggested to cumulatively alter brain structure and compromise neurobehavioural function in the long-term. However, the underlying mechanisms whereby repeated long-term sub-concussion induces cerebral structural and neurobehavioural changes are currently unknown. Here, we utilised an established rat model to investigate the effects of repeated sub-concussion on size of lateral ventricles, cerebrovascular blood–brain barrier (BBB) integrity, neuroinflammation, oxidative stress, and biochemical distribution. Following repeated sub-concussion 3 days per week for 2 weeks, the rats showed significantly enlarged lateral ventricles compared with the rats receiving sham-only procedure. The sub-concussive rats also presented significant BBB dysfunction in the cerebral cortex and hippocampal formation, whilst neuromotor function assessed by beamwalk and rotarod tests were comparable to the sham rats. Immunofluorescent and spectroscopic microscopy analyses revealed no significant changes in neuroinflammation, oxidative stress, lipid distribution or protein aggregation, within the hippocampus and cortex. These data collectively indicate that repeated sub-concussion for 2 weeks induce significant ventriculomegaly and BBB disruption, preceding neuromotor deficits.

Protocatechuic Acid Protects Platelets from Apoptosis via Inhibiting Oxidative Stress-Mediated PI3K/Akt/GSK3β Signaling

2021 ◽  
Author(s):  
Fuli Ya ◽  
Kongyao Li ◽  
Hong Chen ◽  
Zezhong Tian ◽  
Die Fan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Protocatechuic Acid ◽  
Human Platelets ◽  
Ros Generation ◽  
Inhibitory Effects ◽  
Platelet Apoptosis ◽  
Phosphatidylserine Exposure ◽  
Underlying Mechanisms

AbstractOxidative stress plays crucial roles in initiating platelet apoptosis that facilitates the progression of cardiovascular diseases (CVDs). Protocatechuic acid (PCA), a major metabolite of anthocyanin cyanidin-3-O-β-glucoside (Cy-3-g), exerts cardioprotective effects. However, underlying mechanisms responsible for such effects remain unclear. Here, we investigate the effect of PCA on platelet apoptosis and the underlying mechanisms in vitro. Isolated human platelets were treated with hydrogen peroxide (H2O2) to induce apoptosis with or without pretreatment with PCA. We found that PCA dose-dependently inhibited H2O2-induced platelet apoptosis by decreasing the dissipation of mitochondrial membrane potential, activation of caspase-9 and caspase-3, and decreasing phosphatidylserine exposure. Additionally, the distributions of Bax, Bcl-xL, and cytochrome c mediated by H2O2 in the mitochondria and the cytosol were also modulated by PCA treatment. Moreover, the inhibitory effects of PCA on platelet caspase-3 cleavage and phosphatidylserine exposure were mainly mediated by downregulating PI3K/Akt/GSK3β signaling. Furthermore, PCA dose-dependently decreased reactive oxygen species (ROS) generation and the intracellular Ca2+ concentration in platelets in response to H2O2. N-Acetyl cysteine (NAC), a ROS scavenger, markedly abolished H2O2-stimulated PI3K/Akt/GSK3β signaling, caspase-3 activation, and phosphatidylserine exposure. The combination of NAC and PCA did not show significant additive inhibitory effects on PI3K/Akt/GSK3β signaling and platelet apoptosis. Thus, our results suggest that PCA protects platelets from oxidative stress-induced apoptosis through downregulating ROS-mediated PI3K/Akt/GSK3β signaling, which may be responsible for cardioprotective roles of PCA in CVDs.

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