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ABSTRACT: Chronic exposure to tire rubber-derived contaminant 6PPD-quinone impairs transcriptome in male mice testis

PROVIDER: PRJNA1068248 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27759056_1.fastq.gz	Fastqsanger.gz
	SRR27759056_2.fastq.gz	Fastqsanger.gz
	SRR27759057_1.fastq.gz	Fastqsanger.gz
	SRR27759057_2.fastq.gz	Fastqsanger.gz
	SRR27759058_1.fastq.gz	Fastqsanger.gz

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Evaluating the bioactivity of the ubiquitous tire preservative 6PPD and degradant, 6PPD-quinone

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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Evaluating the bioactivity of the ubiquitous tire preservative 6PPD and degradant, 6PPD-quinone

Project description:Evaluating the bioactivity of the ubiquitous tire preservative 6PPD and degradant, 6PPD-quinone

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6PPD induces cerebrovascular defects by triggering oxidative stress and ferroptosis in zebrafish

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.

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Project description:6PPD-quinone exposure in coho salmon embryos

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Gestational and lactational exposure to gossypol alters the testis transcriptome

Project description:Reproductive capacity can be altered by challenges experienced during critical periods of development, including fetal development and early neonatal life. Gossypol is a polyphenolic compound, commonly found in seeds of cotton plants, that impairs male reproduction. In this study, we investigated whether the exposure to gossypol in utero and during lactation alters testis development and testis gene expression in sheep.

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Project description:Mixture toxicity of 6PPD-quinone and polystyrene nanoplastics in zebrafish

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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.

2025-08-15 | GSE302559 | GEO

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