Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effects of Medwakh Smoking on Oxidative Stress and Inflammation Among Youth in UAE using Liquid chromatography-mass spectrometry

ABSTRACT: Oxidative stress and inflammation are closely related, and inter-dependent pathophysiological processes. Oxidative stress plays a key role in the pathophysiology of several chronic inflammatory conditions that causes cellular alterations such as lipid damage, increase of cell permeability, apoptosis/cell death, alteration in growth factors, and signaling pathways.An imbalance between the production of reactive oxygen species (ROS) and their neutralization by the antioxidant system results in the onset of oxidative stress which subsequently leads to the release of chronic inflammatory mediators such as pro-inflammatory cytokines, which causes damages to DNA, proteins, and lipids.LC-MSMS is widely used for non-targeted and non-invasive metabolomics of biological samples including saliva in a variety of conditions such as inflammatory conditions, cancers, diabetes, etc. However, to the best of our knowledge, there are currently no metabolomics-based studies identifying salivary biomarkers associated with inflammation and oxidative stress utilizing HPLC-ESI-QTOF-MS. Therefore, in this study, we aim to discover the biochemical and physiological changes induced by medwak smoking and explore the metabolomics profile of medwak smokers with a focus on the markers of oxidative stress and inflammation in comparison to nonsmokers.

ORGANISM(S): Human Homo Sapiens

TISSUE(S): Saliva

DISEASE(S): Oxidative Stress

SUBMITTER: Aghila Rani K.G

PROVIDER: ST002211 | MetabolomicsWorkbench | Mon Jun 20 00:00:00 BST 2022

REPOSITORIES: MetabolomicsWorkbench

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	mwtab	Other

Items per page:

1 - 1 of 1

Similar Datasets

Cystic fibrosis Airway primary epithelial cells in air-liquid interrface culture show abnormal inflammation and lipid metabolism related RNA expresssion compared to non-CF

Project description:A deficiency in cystic fibrosis transmembrane conductance regulator (CFTR) function in cystic fibrosis (CF) leads to chronic lung disease. However, the molecular mechanisms are not well understood and therapies that can help all patients remain elusive. CF is associated with abnormalities in fatty acids, ceramides and cholesterol, therefore we examined the impact of CFTR deficiency on lipid metabolism and pro-inflammatory signaling in airway epithelium using mass spectrometric, protein array and RNAseq analyses. We observed a striking imbalance in fatty acid and ceramide metabolism, associated with chronic oxidative stress under basal conditions in CF mouse lung and well differentiated bronchial epithelial cell cultures of CFTR knock out pig and CF patients. Cell autonomous features of all three CF models included high ratios of ω-6- to ω-3-polyunsaturated fatty acids and long- to very long- chain ceramide species (LCC/VLCC). The anti-oxidants glutathione (GSH) and deferoxamine partially corrected the lipid profile indicating that oxidative stress may promote the lipid abnormalities. CFTR-targeted modulators reduced the lipid imbalance and apparent oxidative stress, confirming the CFTR dependence of lipid ratios. RNA sequencing and protein array analysis revealed higher expression and shedding of cytokines and growth factors from CF epithelial cells compared to non-CF cells, consistent with sterile inflammation and tissue remodeling under basal conditions. Treatment with antioxidants or CFTR modulators that mimic the approved combination therapies, Orkambi and Trikafta, did not suppress the inflammatory phenotype. These results suggest that anti-inflammatory therapies may provide additional benefit for CF patients taking CFTR modulator drugs.

2021-01-01 | GSE154802 | GEO

Human Bronchoalveolar Lavage Cells Gene Expression After Exposure to Increasing Doses of Ozone

2015-06-15 | GSE58682 | GEO

Long-term exposure to cold plasma-generated ROS âan in vitro model for redox-related diseases of the skin

Project description:Oxidative stress illustrates an imbalance between radical formation and removal. Frequent redox stress is critically involved in a variety of human pathologies including cancer, psoriasis, and chronic wounds. However, reactive species pursue a dual role being involved in signaling on the one hand and oxidative damage on the other. Using a HaCaT keratinocyte cell culture model, we here aimed at investigating the cellular and transcriptional response to periodic, low dose oxidative challenge over three months. Chronic redox stress was generated by frequent incubation with cold physical plasma treated cell culture medium. Using mRNA microarray technology, we found both acute ROS stress responses as well as numerous adaptions on the transcriptional level and over several weeks of redox challenge. This included an altered expression of 260 genes that function in inflammation and redox homeostasis, such as, signaling molecules, cytokines, and anti-oxidant enzymes. Apoptotic signaling was affected to a minor extend, especially in p53 down-stream targets. Strikingly, the anti-apoptotic heat shock protein HSP27 was strongly upregulated. These results suggest a variety of adaptive responses relating involved a number of cellular processes elicited by frequent redox stress over several months. They may help to better understand inflammatory responses in redox related diseases and possibly allow uncovering new biomarkers of ROS-stress. Microarrays were used to analyze and investigate the biological effects of repeated exposure of cold physical plasma on human HaCaT keratinocytes. Using an argon plasma jet kinpen, regulated transcripts were analyzed and further described in Schmidt et al. (submittes): âLong-term exposure to cold plasma-generated ROS âan in vitro model for redox-related diseases of the skinâ. HaCaT keratinocytes exposed to plasma treated medium - time course

2015-11-11 | E-GEOD-74876 | biostudies-arrayexpress

Human Bronchoalveolar Lavage Cells Gene Expression After Exposure to Increasing Doses of Ozone

Project description:Ozone, the major component of air pollution, is an oxidant gas. Inhalation of high ambient levels of ozone causes oxidative stress and airway inflammation. To assess the biological responses of airway inflammatory cells to ozone-induced oxidative stress, we examined the gene expression of airway inflammatory cells in response to inhalation of ozone. Nineteen subjects, with and without asthma, were exposed to clean air (0 ppb), low (100ppb), and high (200ppb) ambient levels of ozone for 4 hours on three separate occasions in a climate-controlled chamber followed by bronchoscopy with bronchoalveolar lavage (BAL) 20 hours after the end of exposure in a repeated measure design. The BAL cells mRNA expression was examined using Affymetrix GeneChip Microarray.

2015-06-15 | E-GEOD-58682 | biostudies-arrayexpress

Quercetin suppresses immune cell accumulation and improves mitochondrial gene expression in epididymal adipose tissue of diet-induced obese mice

Project description:We examined the effect of quercetin on the gene expression and function of epididymal adipose tissue (EAT) in Western diet-induced obese mice. Quercetin suppressed the increase in the number of macrophages and the decrease in the ratio of CD4+ to CD8+ T cells in EAT, and the elevation of plasma leptin and TNFÎ± levels in mice fed the Western diet. Comprehensive gene expression analysis revealed that quercetin suppressed gene expression associated with the accumulation and activation of immune cells, including macrophages and lymphocytes in EAT. It also improved the expression of the oxidative stress-sensitive transcription factor NFÎºB, NADPH oxidases, and antioxidant enzymes. Quercetin markedly increased gene expression associated with mitochondrial oxidative phosphorylation and mitochondrial DNA Quercetin most likely universally suppresses the accumulation and activation of immune cells, including anti-inflammatory cells, whereas it specifically increased gene expression associated with mitochondrial oxidative phosphorylation. Suppression of oxidative stress and NFÎºB activity likely contributed to the prevention of the accumulation and activation of immune cells and resulting chronic inflammation. Quercetin most likely universally suppresses the accumulation and activation of immune cells, including anti-inflammatory cells, whereas it specifically increased gene expression associated with mitochondrial oxidative phosphorylation. Suppression of oxidative stress and NFÎºB activity likely contributed to the prevention of the accumulation and activation of immune cells and resulting chronic inflammation. C57BL/6J mice were fed a control diet; a Western diet high in fat, cholesterol, and sucrose; or the same Western diet containing 0.05% quercetin for 18 weeks.

2016-02-25 | E-GEOD-71367 | biostudies-arrayexpress

Label-free comparative data independent (DIA) nanoLC-MS/MS analysis of protein expression profiles of mouse primary dendritic cells (DC) from B6 mice on normal and high fructose/high fat (HFHF) diet

Project description:A diet rich in saturated fat and carbohydrates causes a low-grade chronic inflammation in several organs including nonalcoholic steatohepatitis. The environment-driven lipotocicity and glucotoxicity induce tissue damage, which promotes dendritic cell adjuvanticity, and supports an MHC-class-II immunopeptidome enriched in peptides derived from proteins involved in cellular metabolism, oxidative phosphorylation and molecular cellular responses to oxidative stress. To investigate the impact of metabolic syndrome on the whole cellular proteome of antigen presenting cells (APCs) we isolated six biological replicates consisted of total proteomic extracts DCs lysates from B6 mice on normal and high fructose/high fat (HFHF) diet and employed a quantitative label-free data independent (DIA) nanoLC-MS/MS analysis of redox stress mediated changes in the protein expression profiles in HFHF vs normal diet. The LFQ DIA analysis of cellular proteomics changes induced by HFHF diet in the DCs highlighted the involvement of proteins associated with cellular pathways involved in lipid and carbohydrate metabolism, oxidative phosphorylation, cell death and inflammation. Altogether depicting an image of cells under metabolic and oxidative stress with up-regulated inflammatory pathways.

2022-08-22 | PXD026190 | Pride

TDP-43 aggregation induced by oxidative stress causes global mitochondrial imbalance in ALS

Project description:TDP-43 aggregation induced by oxidative stress causes global mitochondrial imbalance in ALS

| PRJNA523364 | ENA

Fumaric acid esters can block pro-inflammatory actions of human CRP and ameliorate metabolic disturbances in transgenic spontaneously hypertensive rats

Project description:Inflammation and oxidative stress have been implicated in the pathogenesis of metabolic disturbances. Esters of fumaric acid, mainly dimethyl fumarate (DMF), exhibit immunomodulatory, anti-inflammatory, and anti-oxidative effects. In the current study, we tested the hypothesis that fumaric acid ester treatment of an animal model of inflammation and metabolic syndrome, the spontaneously hypertensive rat transgenically expressing human C-reactive protein (SHR-CRP), will ameliorate inflammation, oxidative stress, and metabolic disturbances.

2015-12-31 | E-MTAB-2406 | biostudies-arrayexpress

IDENTIFICATION OF A NOVEL GENETIC PROGRAM AT THE INITIATION OF COLON CANCER DEVELOPMENT.

Project description:As a result of a chronic inflammation or in response to the constitutive activation of the beta-catenin pathway, the generation of reactive oxygen species causes telomere attrition and triggers intestinal cell commitment into a senescence program. Nonetheless, such events are known to promote their neoplastic transformation, suggesting that the escape from oxidative stress-induced senescence favors the emergence of deleterious cells. By setting up an in vitro model, we demonstrated that the escape of human colonic epithelial cells from chronic inflammation-induced senescence lied on the activation of a specific genetic program.

2018-06-30 | GSE70170 | GEO

Expression profiling of human early myotubes after exposure to RXF or SKR conditioned media

Project description:Cachexia is a devastating muscle wasting syndrome that occurs in patients suffering from chronic diseases, most commonly observed in 80% of advanced cancer patients. One of the primary causes of cachexia-associated morbidity and mortality is involuntary muscle wasting. And while many cachexia patients show hypermetabolism, its causative role in muscles had remained unclear. To understand the molecular basis of this muscle wasting, accurate models of cachexia are necessary. Using transcriptomics and cytokine profiling of human muscle stem cell-based models and human cancer-induced cachexia models in mice, we found that cachectic cancer cells secreted many inflammatory factors which rapidly led to higher levels of fatty acid metabolism and the activation of a p38 stress response signature, before the cachectic muscle wasting is manifested. Metabolomics profiling revealed that factors secreted by cachectic cancer cells rapidly induce excessive fatty acid oxidation in human myotubes, leading to oxidative stress, p38 activation, and impaired muscle growth. Pharmacological blockade of fatty acid oxidation not only rescued human myotubes, but also significantly improved muscle mass and total weight in cancer cachexia models in vivo. Therefore, fatty acid-induced oxidative stress could be targeted to prevent cancer cachexia.

2016-05-01 | GSE80080 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data