Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1171555 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30947514_1.fastq.gz | Fastqsanger.gz | |||
| SRR30947514_2.fastq.gz | Fastqsanger.gz | |||
| SRR30947515_1.fastq.gz | Fastqsanger.gz | |||
| SRR30947515_2.fastq.gz | Fastqsanger.gz | |||
| SRR30947516_1.fastq.gz | Fastqsanger.gz |
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Project description:N-(1,3-dimethylbutyl)-N′-phenyl-p-phenylenediamine (6PPD), which is widely used as an antiozonant in rubber tires, has recently got much attention for its acute aquatic toxicity. However, the developmental toxicity of 6PPD in cerebrovascular network remains unknown. Here, we investigated the effects of 6PPD exposure in cerebral vascular using the larvae of zebrafish. 6PPD would not affect the body length and shape of zebrafish larvae at the concentrations ranging from 20 μg/L to 1000 μg/L. 6PPD induced developmental defects in the brain in a concentration-dependent manner. The trunk vascular development would not be affected while the cerebrovascular network was disrupted upon 6PPD exposure. 6PPD would trigger excessive Reactive Oxygen Species (ROS) in the brain, indicating abnormal oxidative stress. Mechanistically, brain-specific transcriptome analysis showed that 6PPD could potentially cause the blockage of arachidonic acid (AA) metabolism-related genes and the upregulation of ferroptosis-related genes. Besides, treatment with ferroptosis inhibitor N-Acetyl-L-cysteine (NAC) attenuated oxidative damage and improved the construction of cerebrovascular network upon 6PPD exposure. Moreover, using a human vascular endothelial cell line, we further confirmed that 6PPD could trigger abnormal oxidative stress and defective expansion capacity, implying the conserved toxicity cross species. These findings are useful for the elucidation of toxicity underlying 6PPD in cerebrovascular systems of both zebrafish and humans.
2025-05-30 | GSE279887 | GEO
Project description:N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine quinone (6PPD-quinone; 6PPD-Q), a transformation product of an antiozonant chemical widely used in automobile tires (6PPD; N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine) was identified as the causative agent for pre-spawn mortality in coho salmon resulting from exposure to stormwater run-off. This study employed a 24 h, 96-well plate based, exposure to larval fathead minnows (5 days post-fertilization) to examine the effects of 6PPD and 6PPD-Q exposure on global gene expression. Concentration-response modeling of the resulting gene expression changes identified a transcriptomic point of departure of 1.3 uM for 6PPD and 2.5 uM for 6PPD-Q, although they are effectively equivalent considering the range of uncertainty. Examination of the functional roles of differentially expressed genes provided little insight into the mechanism of idiosyncratic toxicity observed in coho salmon and certain other salmonid species. Overall, larval fathead minnows do not appear sensitive to the same mechanisms.
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Project description:To understand molecular mechanisms of the chronic, sublethal toxicity of 2,4,6-trinitrotoluene (TNT), a widely used ordnance compound of public concerns, we constructed a microarray consisting of 4,032 cDNA isolated from the earthworm Eisenia fetida using the suppressive subtractive hybridization technique. Worms were exposed to a gradient of TNT-spiked soil for 28 days. Based on the reproduction response to TNT, four treatments, i.e., control, 7, 35 and 139 ppm, were selected for gene expression studies. Keywords: Sublethal toxicity of TNT (dose-response) to earthworm (Eisenia fetida)
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Project description:To understand molecular mechanisms of the joint effects of 2,4,6-trinitrotoluene (TNT) and hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX), both widely used ordnance compounds, we constructed a microarray consisting of 4,032 cDNA isolated from the earthworm Eisenia fetida using the suppressive subtractive hybridization technique. Worms were exposed to TNT-, RDX-, or TNT+RDX-spiked soil for 28 days (TNT 50 mg/kg, RDX 30 mg/kg). Keywords: Combined toxicity of TNT and RDX to earthworm (Eisenia fetida)
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Project description:N-(1,3-Dimethyl butyl)-N′-phenyl-phenylenediamine-quinone (6ppd-quinone) is of emerging concern due to its widespread presence and toxicity to aquatic species. The chemical has been detected in human biofluids though little is known about its effects on human tissues. The objective of this study was to increase understanding of 6ppd-quinone’s potential human health effects by deriving transcriptomic points of departure (tPOD) values in two human cell lines using the TPD-seq workflow. An EC20 for cytotoxicity was calculated for Caco-2 (104µg/L) but not for HepG2 cells. Even in the absence of cytotoxicity, tPOD values (20th gene, 10th percentile, mode) were calculated in Caco-2 (6.5-25µg/L) and HepG2 (0.36-35µg/L) cells. These ranges capture values from 16 statistical and bioinformatic tests that examined mapping methods (CLC and Deplexer), algorithms (Limma and DESeq2), and filters (log2FC and BMR). The most common and sensitive genes with calculable benchmark doses (BMDs) in Caco-2 (DPF2, CD44, PGAP1, GDF15, H4C16) and HepG2 (SLC5A3, DKK1, ARG2, PHLDA1, TM4SF1) cells are listed. Pathway BMDs were also calculated for Caco-2 (systemic lupus erythematosus, 9.7-18µg/L; alcoholism, 9.7-20µg/L; viral carcinogenesis, 9.3-18.1µg/L), and HepG2 (metabolic pathways, 50-60µg/L) cells. These findings highlight TPD-seq as an efficient workflow to yield quantitative and mechanistic data relevant for human health risk assessment.
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