Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1129278 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29646202_1.fastq.gz | Fastqsanger.gz | |||
| SRR29646202_2.fastq.gz | Fastqsanger.gz | |||
| SRR29646203_1.fastq.gz | Fastqsanger.gz | |||
| SRR29646203_2.fastq.gz | Fastqsanger.gz | |||
| SRR29646204_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 168 |
Similar Datasets
Project description:<p> Microplastics pollution is prevalent in livestock environments, especially in ruminant feed. Exposure to microplastics can damage the gastrointestinal barrier, alter microbiota, and lead to organ damage. Despite its impact on cattle farming and potential human health risks, the effects of microplastics on cattle remain unexplored. This study investigates microplastic-induced toxicity through the rumen microbiota-gut-liver axis in beef cattle. We found that Microplastic exposure reduced body weight gain and liver development, induced pathological changes in the liver, increased lipopolysaccharide (LPS) levels in both blood and muscle, and triggered systemic inflammation, particularly affecting the liver. Alterations in rumen microbiota and metabolites were associated with liver inflammation. Furthermore, microplastics damaged the rumen, jejunum, and colon barriers, resulting in microbial dysbiosis, metabolic disorders, and activation of LPS synthesis pathways. Metabolomics of rumen fluid identified key metabolites-including 4-Fluoro-3-phenoxybenzoic acid and Isovalerylglutamic acid, which correlated with inflammatory markers (LPS, TNF-α, and IL-6). Transcriptomic analysis further corroborated inflammation in blood and liver, revealing activation of NF-κB pathway primarily via Toll-like receptor 4 (TLR4), which inhibited hepatocyte proliferation and promoted apoptosis.</p><p> Collectively, this study reveals that microplastics impair cattle liver function via the rumen microbiota-gut-liver axis. Microplastics disrupt the rumen microbiota, activate the LPS synthesis, and damage the intestinal barrier, allowing LPS to enter the bloodstream and subsequent liver damage. Additionally, LPS will also remain in the muscles, which to some extent exacerbates the risk of LPS in meat products to human health. Reducing the use of plastic products in animal husbandry and modulation of the rumen microbiota may provide a potential strategy to alleviate microplastic-induced hepatotoxicity. </p>
2025-09-08 | MTBLS12958 | MetaboLights
Project description:<p>Microplastics pollution is prevalent in livestock environments, especially in ruminant feed. Exposure to microplastics can damage the gastrointestinal barrier, alter microbiota, and lead to organ damage. Despite its impact on cattle farming and potential human health risks, the effects of microplastics on cattle remain unexplored. This study investigates microplastic-induced toxicity through the rumen microbiota-gut-liver axis in beef cattle. We found that Microplastic exposure reduced body weight gain and liver development, induced pathological changes in the liver, increased lipopolysaccharide (LPS) levels in both blood and muscle, and triggered systemic inflammation, particularly affecting the liver. Alterations in rumen microbiota and metabolites were associated with liver inflammation. Furthermore, microplastics damaged the rumen, jejunum, and colon barriers, resulting in microbial dysbiosis, metabolic disorders, and activation of LPS synthesis pathways. Metabolomics of rumen fluid identified key metabolites-including 4-Fluoro-3-phenoxybenzoic acid and Isovalerylglutamic acid, which correlated with inflammatory markers (LPS, TNF-α, and IL-6). Transcriptomic analysis further corroborated inflammation in blood and liver, revealing activation of NF-κB pathway primarily via Toll-like receptor 4 (TLR4), which inhibited hepatocyte proliferation and promoted apoptosis.</p><p>Collectively, this study reveals that microplastics impair cattle liver function via the rumen microbiota-gut-liver axis. Microplastics disrupt the rumen microbiota, activate the LPS synthesis, and damage the intestinal barrier, allowing LPS to enter the bloodstream and subsequent liver damage. Additionally, LPS will also remain in the muscles, which to some extent exacerbates the risk of LPS in meat products to human health. Reducing the use of plastic products in animal husbandry and modulation of the rumen microbiota may provide a potential strategy to alleviate microplastic-induced hepatotoxicity. </p>
2025-09-08 | MTBLS12959 | MetaboLights
Project description:To assess the impact of surface water across the Hun River, several sampling sites located in the mainstream and the tributary were selected representative of pollution gradient and different pollution source. Male adult zebrafish were exposed to surface water from seven sites for 4 days. The obiectives of the study was to evaluate the ability of transcriptomic profiles exposed to surface water to determine the potential biological effects, to differentiate different pollution source, and to identify the toxic components.
2017-04-01 | GSE92330 | GEO
Project description:To assess the impact of surface water across the Hun River, several sampling sites located in the mainstream and the tributary were selected representative of pollution gradient and different pollution source. Male adult zebrafish were exposed to surface water from seven sites for 4 days. The obiectives of the study was to evaluate the ability of transcriptomic profiles exposed to surface water to determine the potential biological effects, to differentiate different pollution source, and to identify the toxic components.
2017-12-19 | GSE108227 | GEO
Project description:To assess the impact of surface water across the Hun River, several sampling sites located in the mainstream and the tributary were selected representative of pollution gradient and different pollution source. Human mesenchymal stem cells were exposed to organic extracts of surface water from six sites for 2 days. Microarrays were used to measure the gene expression. And the gene expression profiles were used to evaluate the ability of determine the potential biological effects, to differentiate different pollution source, and to identify the toxic components.
2018-06-01 | GSE110310 | GEO
Project description:Polyethylene microplastics are pervasive environmental pollutants that pose potential risks to aquatic organisms. This study investigates the effects of polyethylene microplastics on zebrafish (Danio rerio) embryo development, with a focus on whether the chorion, a protective barrier surrounding the embryo, is effective in blocking polyethylene penetration. Contrary to previous findings that suggested the chorion could prevent larger microplastics (>0.7 µm) from entering, our study demonstrates that polyethylene particles sized 1-4 µm can still negatively impact embryo development without dechorionation. Embryos were exposed to polyethylene at concentrations of 0.01, 0.1, and 1 mg/L, followed by RNA sequencing to assess gene expression changes. Despite no significant differences in survival, hatching, or body length between control and treated groups, a significant reduction in heart rate was observed at higher concentrations, indicating potential sub-lethal cardiotoxicity. Further, qRT-PCR validation confirmed significant downregulation of key heart development-related genes, particularly fbln1 and fn1b, in polyethylene-exposed embryos. Additionally, polyethylene exposure also impacted Daphnia magna, reducing heart rate and delaying growth. These findings highlight the ability of polyethylene microplastics to penetrate natural barriers such as the chorion and induce physiological and developmental changes. Our results emphasize the need for further research into the long-term effects of microplastic exposure on aquatic ecosystems.
2025-11-30 | GSE281865 | GEO