Metabolomics analysis for gut bacteria after pesticide exposure
Ontology highlight
ABSTRACT:
INSTRUMENT(S): LC-QE Orbitrap MS
ORGANISM(S): Human Gut Bacteria
SUBMITTER: 
Jiangjiang Zhu
PROVIDER: MSV000095526 | MassIVE | Tue Aug 06 08:10:00 BST 2024
REPOSITORIES: MassIVE
Similar Datasets
Project description:raw data for lipidomics analysis in gut bacteria after pesticide exposure.
2024-08-07 | MSV000095539 | MassIVE
Project description:We tested the hypothesis that differential gene expression in whole blood will reveal candidate blood biomarkers for exposure to agricultural pesticides and herbicides. Blood gene expression in male Latino farmworkers, where chronic pesticide exposure is occupational, was compared to blood gene expression in age and gender matched Latino manual workers. We identified an expression signature for farmwork, differential expression in genes that correlated with levels of urinary pesticide metabolites, alterations in axonal guidance pathways and statistical models that link farmworker differential expression to Parkinson's disease.
2019-12-31 | GSE30335 | GEO
Project description:Pesticides are essential in modern agriculture but raise concerns about long-term metabolic effects, particularly through nuclear receptor activation. This study examines the impact of chronic exposure to a mixture of five pesticides (dieldrin, propiconazole, boscalid, bupirimate, and pendimethalin) with or without tributyltin (TBT) on glucose and lipid metabolism in mice, focusing on the role of the constitutive androstane receptor (CAR) and pregnane X receptor (PXR). TBT was included for its strong affinity for RXR, a key heterodimerization partner of CAR and PXR, to assess whether RXR activation modulates or amplifies the metabolic effects of pesticide exposure. Results showed that pesticide exposure at NOAEL levels altered CAR and PXR dependent metabolic pathways. CAR knockout mice exhibited reduced free fatty acids and fasting glycemia, while PXR activation led to lower peak glycemia in oral glucose tolerance tests. Transcriptomic analysis identified disrupted pathways linked to glucose uptake and insulin sensitivity. These findings suggest that low-dose pesticide exposure can subtly affect metabolism via nuclear receptor interactions. The inclusion of TBT emphases RXR’s role in metabolic regulation. Overall, the study underscores the need to consider cocktail effects in risk assessment.
2025-09-01 | GSE297527 | GEO
Project description:Prenatal environmental conditions may influence disease risk in later life. We previously found a gene-environment interaction between the paraoxonase 1 (PON1) Q192R genotype and prenatal pesticide exposure leading to a cardio-metabolic risk profile at school age. However, the molecular mechanisms involved have not yet been resolved. It has been hypothesized that epigenetics might be involved. The aim of the present study was to investigate whether DNA methylation patterns in blood cells were related to prenatal pesticide exposure level, PON1 Q192R genotype, and associated metabolic effects observed in the children. Whole blood DNA methylation patterns in 48 children (6-11 years of age), whose mothers were occupationally unexposed or exposed to pesticides early in pregnancy, were determined by Illumina 450K methylation arrays. A specific methylation profile was observed in prenatally pesticide exposed children carrying the PON1 192R allele. Differentially methylated genes were enriched in several neuroendocrine signaling pathways including dopamine-DARPP32 feedback (appetite, reward pathways), corticotrophin releasing hormone signalling, nNOS, neuregulin signalling, mTOR signalling and type II diabetes mellitus signalling suggesting a possible link with the metabolic effects observed in these children. Furthermore, we were able to identify possible candidate genes which mediate the effect between pesticide exposure, leptin levels, delta BMI Z-score, and body fat percentage. In conclusion, DNA methylation may be an underlying mechanism explaining cardio-metabolic health outcomes in children that are prenatally exposed to pesticides and carrier of the PON1 192R allele.
2017-05-01 | GSE90117 | GEO
Project description:Placental Functional Networks Linking Developmental Pesticide Exposure and Offspring Neurodevelopment
| PRJNA1026726 | ENA
Project description:Accumulating evidence suggests that paternal environmental factors have epigenetic effects on sperm and influence offspring. Neonicotinoid pesticides, which are widely used around the world, are known to affect offspring phenotypes through maternal exposure in mice, but the effect of the paternal exposure remains unknown.The main purpose of this study was to estimate the neurobehavioral effects on offspring mice resulting from paternal exposure to the neonicotinoid pesticide clothianidin (CLO).Hippocampal RNA sequence data revealed that paternal CLO exposure altered the expression of genes related to the nervous system in male offspring, affecting pathways such as axonal guidance signaling, synaptogenesis signaling pathway, and calcium signaling.
2024-11-07 | GSE281282 | GEO
Project description:Consumers are exposed through food intake to a cocktail of pesticides at low doses. Epidemiological evidence suggested a link between pesticide exposure and the development of the metabolic syndrome. We used a mouse model to mimic consumer exposure and assessed the metabolic consequences of a chronic dietary exposure to a cocktail of 6 commonly used pesticides (boscalid, captan, chlorpyrifos, thiofanate, thiacloprid and ziram) at non-toxic doses (acceptable daily intake ADI). One year of exposure induced body weight and adiposity gain, hepatic steatosis and glucose intolerance in males. Females did not display significant changes in body weight but displayed fasted hyperglycemia and perturbations of gut-microbiota related urinary metabolites. Exposure of mice invalidated for the constitutive androstane receptor (CAR) demonstrated that this nuclear receptor was involved in the observed sexual dimorphic response to pesticide exposure. These results demonstrate for the first time that chronic dietary exposure to a pesticide cocktail at the ADI levels induces metabolic perturbations favouring obesity and diabetic state and raise the questions of the relevance of the ADI levels of individual pesticides when present in mixture.
2018-07-05 | GSE101405 | GEO
Project description:The interplay between pathogens and hosts has been studied for decades using targeted approaches such as the analysis of mutants and host immunological responses. Although much has been learned from such studies, they focus on individual pathways and fail to reveal the global effects of infection on the host. To alleviate this issue, high-throughput methods such as transcriptomics and proteomics have been used to study host-pathogen interactions. Recently, metabolomics was established as a new method to study changes in the biochemical composition of host tissues. We report a metabolomics study of Salmonella enterica serovar Typhimurium infection. We used Fourier Transform Ion Cyclotron Resonance Mass Spectrometry with Direct Infusion to reveal that dozens of host metabolic pathways are affected by Salmonella in a murine infection model. In particular, multiple host hormone pathways are disrupted. Our results identify unappreciated effects of infection on host metabolism and shed light on mechanisms used by Salmonella to cause disease, and by the host to counter infection. Female C57BL/6 mice were infected with Salmonella enterica serovar Typhimurium SL1344 cells by oral gavage. Feces and livers were collected and metabolites extracted using acetonitrile. For experiments with feces, samples were collected from 4 mice before and after infection. For liver experiments, 11 uninfected and 11 infected mice were used. Samples were combined into 3 groups of 3-4 mice each, resulting in the analysis of 3 group samples of uninfected and 3 of infected mice. Extracts were infused into a 12-T Apex-Qe hybrid quadrupole-FT-ICR mass spectrometer equipped with an Apollo II electrospray ionization source, a quadrupole mass filter and a hexapole collision cell. Raw mass spectrometry data were processed as described elsewhere (Han et al. 2008. Metabolomics. 4:128-140 [PMID 19081807]). To identify differences in metabolite composition between uninfected and infected samples, we filtered the list of masses for metabolites which were present on one set of samples but not the other. Additionally, we calculated the ratios between averaged intensities of metabolites from uninfected and infected mice. To assign possible metabolite identities, monoisotopic neutral masses of interest were queried against MassTrix (http://masstrix.org). Masses were searched against the Mus musculus database within a mass error of 3 ppm. Data were analyzed by unpaired t tests with 95% confidence intervals.
2011-02-08 | E-GEOD-21720 | biostudies-arrayexpress
Project description:<div>BACKGROUND: Epidemiological evidence suggests a link between pesticide exposure and the development of metabolic diseases. However, most experimental studies have evaluated the metabolic effects of pesticides using individual molecules, often at non relevant doses or in combination with other risk factors such as high fat diets.<br></div><div>OBJECTIVES: We aimed to evaluate, in mice, the metabolic consequences of chronic dietary exposure to a pesticide mixture at non-toxic doses, relevant to consumers’ risk assessment.<br></div> METHODS: A mixture of six pesticides commonly used in France i.e. boscalid, captan, chlorpyrifos, thiofanate, thiacloprid, and ziram was incorporated in a standard chow diet, at doses exposing mice to the acceptable daily intake (ADI) of each pesticide. Wild-type (WT) and Constitutive Androstane Receptor knock-out (CAR-/-) C57Bl6/J male and female mice were exposed for 52 weeks. We assessed metabolic parameters (body-weight, food and water consumption, glucose tolerance, urinary metabolome) throughout the experiment. At the end of the experiment, we evaluated liver metabolism (histology, transcriptomics, metabolomics) and pesticide detoxification using LC/MS.<br>RESULTS: In males, pesticide exposure increased body weight and adiposity and induced hepatic steatosis and glucose intolerance. Exposed females exhibited fasted hyperglycaemia, hepatic oxidative stress and perturbations of gut microbiota-related urinary metabolites. The Constitutive Androstane Receptor is involved in the sexually dimorphic response to pesticide exposure.<br><div> CONCLUSIONS: We show for the first time the sexually dimorphic obesogen and diabetogen effects of a chronic dietary exposure to a realistic mixture of pesticides, which are partially mediated through CAR. This raises questions about the relevance of ADI for individual pesticides when present in a mixture.</div><div><br></div><div><b>Untargeted urine UPLC-MS assay</b> protocols and data are reported in the current study <b>MTBLS596</b>.</div><div><br><b>Untargeted urine, plasma and liver NMR assay</b> protocols and data associated to this study are reported in <a href=https://www.ebi.ac.uk/metabolights/mtbls602><b>MTBLS602</b></a>.<br></div>
2019-05-28 | MTBLS596 | MetaboLights
Project description:Pesticides pose a potential threat to bee health, especially in combination with other stressors, like parasites. However, pesticide risk assessment tests them in isolation from other stresses. We tested acute oral doses of three pesticides - glyphosate, Amistar and sulfoxaflor - on the bumblebee, Bombus terrestris, alongside the gut parasite Crithidia bombi. We found no impact of any pesticide on parasite intensity and no impact of sulfoxaflor or glyphosate on survival or weight change. Amistar caused weight loss and 19-41% mortality. Haemoproteome analysis showed various protein dysregulations. The major pathways dysregulated are those involved in insect defences and immune responses, with Amistar having the strongest impact on these. Our results show that while no response can be seen at a whole organism level, MALDI BeeTyping® can detect effects. Mass spectrometry analysis of bee haemolymph represent a pertinent tool to evaluate the stressor impacts on bee health, even at the individual scale.
2023-02-09 | PXD039916 | Pride