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Integrated network toxicology and transcriptomics reveal DIBP and DEP induce hepatic toxicity via ferroptosis

ABSTRACT: Our study comprehensively revealed the molecular mechanisms of hepatotoxicity induced by diethyl phthalate (DEP) and diisobutyl phthalate (DIBP) at the transcriptomic level, providing new experimental evidence for understanding the toxic mechanisms of phthalate esters.

ORGANISM(S): Danio rerio

PROVIDER: GSE332878 | GEO | 2026/09/09

REPOSITORIES: GEO

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Transcriptomics reveal DIBP induce immunotoxicity

Project description:Our study comprehensively revealed the molecular mechanisms of immunotoxicity induced diisobutyl phthalate(DIBP) at the transcriptomic level, providing new experimental evidence forunderstanding the toxic mechanisms of phthalate esters.

2026-09-17 | GSE347089 | GEO

Evaluation of the potential toxicity mechanism of single and combined exposure of dibutyl phthalate and diisobutyl phthalate to zebrafish (Danio rerio) testis based on transcriptomic analysis

Project description:Aquatic organisms are generally exposed to a mixture of phthalate esters (PAEs) that have been shown to induce reproductive toxicity. However, their potential toxicity mechanisms to aquatic organisms remain unclear. Here male zebrafish were exposed to dibutyl phthalate (DBP), diisobutyl phthalate (DiBP) and their mixtures for 30 days, and their effects on plasma sex hormones, testis histology and testis transcriptomics were investigated. DBP, DiBP and their mixtures could induce the disequilibrating ratio of testosterone (T) and plasma estradiol (E2) in plasma. The percentage of spermatozoa (Sz) was significantly decreased by 30.6% under DBP-1133 exposure and 27.8% under Mix-3 exposure, and widen intercellular spaces appeared under DiBP-1038 exposure. Transcriptome sequencing revealed 2795 differentially expressed genes (DEGs) in the DBP-1133 exposure group, 1613 DEGs in the DiBP-1038 exposure group and 4570 DEGs in the Mix-3 exposure group, indicating that the toxicity of combined exposure was higher than that of single exposure. Cytokine-cytokine receptor interaction was associated with the toxicity mechanism of DBP, DiBP and Mix. While GnRH signaling pathway and MAPK signaling pathway were related to the toxicity mechanism of DBP. ECM-receptor interaction, steroid hormone biosynthesis, retinol metabolism and PPAR signaling pathway were associated with the toxicity mechanism of DiBP and Mix.

2021-09-30 | GSE136994 | GEO

Transcriptomic analysis reveals potential mechanisms of toxicity in a combined exposure to dibutyl phthalate and diisobutyl phthalate in zebrafish (Danio rerio) ovary

Project description:Phthalate esters (PAEs), a notable plasticizer, could be prolific contaminants in the aquatic environment, and have been shown to induce reproductive toxicity. However, studies concerning the toxicity towards aquatic species are based upon individual chemicals and the combined toxicity of PAEs to aquatic organisms remains unclear. The aim of this study was to explore the potential toxic mechanism of combined exposure to dibutyl phthalate (DBP) and diisobutyl phthalate (DiBP) in adult female zebrafish ovarian. Zebrafish were exposed to DBP, DiBP and their mixtures for 30 days, and their effects on ovarian histology, plasma sex hormones and ovarian transcriptomics were investigated. The plasma estradiol (E2) levels were significantly decreased 38.9% for DBP-1133 exposure group and 41.0% for DiBP-1038 exposure group. The percentages of late/mature oocyte were also significantly decreased 17.3% in DBP-1133 exposure and 16.2% in DiBP-1038 exposure, while those in combined exposure were not significantly affected. Nonetheless, transcriptome sequencing discovered 2564 differential expressed genes (DEGs) in zebrafish ovary after exposure to the mixtures. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis identified that those DEGs were involved in the neuroactive ligand-receptor interaction, GnRH, progesterone-mediated oocyte maturation, oocyte meiosis and steroid hormone biosynthesis signaling pathways. These results revealed that combined exposure showed potential reproductive toxicity at the molecular level.

2019-08-27 | GSE134345 | GEO

The impact of diethyl phthalate (DEP) on metabolism-related diseases

Project description:The impact of diethyl phthalate (DEP) on metabolism-related diseases

| PRJNA1330281 | ENA

Integrated network toxicology and transcriptomics reveal DIBP and DEP induce hepatic toxicity via ferroptosis

Project description:Integrated network toxicology and transcriptomics reveal DIBP and DEP induce hepatic toxicity via ferroptosis

| PRJNA1469217 | ENA

Cross-Feeding Drives Degradation of Phthalate Ester Plasticizers in a Bacterial Consortium

Project description:A bacterial consortium capable of degrading diethyl phthalate (DEP) was enriched from a biofilm of a polyurethane tubing. The consortium was capable to mineralize DEP as the sole carbon and energy source.

2026-03-20 | PXD073022 | Pride

Transcriptomic responses predict the toxic effect of parental combined exposure to DBP and DiBP on the early development of zebrafish offspring

Project description:Dibutyl phthalate (DBP) and diisobutyl phthalate (DiBP) have been reported to exhibit reproductive toxicity and may pose a threat to their offspring. However, the combined effect of DBP and DiBP on offspring remains unclear, especially for aquatic organisms. The aims of this study were to assess the effects of parental combined exposure to DBP and DiBP on early development of zebrafish offspring, and to explore the potential molecular mechanisms involved. The early developmental indicators and transcriptomic profiles of F1 larvae were examined after parental exposure to DBP, DiBP and their mixtures (Mix) for 30 days. Results showed that parental exposure to DBP and DiBP, alone or in combination, resulted in increasing hatchability at 48 hpf and heart rate at 96 hpf, and affected the malformation and mortality in F1 larvae. Generalized linear model (GLM) indicated that the interactive effects between DBP and DiBP on the mortality and malformation of F1 larvae was antagonistic. The transcriptomic analysis predicted that the molecular mechanisms of parental combined exposure were different from those of either chemical alone, disruption of the molecular function involving unfolded protein binding, E-box binding and photoreceptor activity in F1 larvae could be the mechanism of action after parental combined exposure.

2020-12-29 | GSE147715 | GEO

Mammary transcriptome of rats treated with low-dose environmental chemicals from birth to adulthood

Project description:Exposure to common environmental chemicals, including those found in personal care products has been linked to mammary cancer at high doses in animal models. Their effects at low doses at levels comparable to human exposure remain poorly understood. Using a Sprague-Dawley rat model, we investigated the effects of three prevalently used environmental chemicals – diethyl phthalate (DEP), methyl paraben (MPB), triclosan (TCS) – and their mixture (MIX) on the transcriptome of normal developing mammary at levels mimicking human exposure. Rats were exposed from birth to adulthood in parous and nulliparous settings. We used affymetrix arrays to assess the influence of diethyl phthalate (DEP), methyl paraben (MPB), triclosan (TCS) and their mixture (MIX) on global gene expression profiles in rat mammary tissues, using doses comparable to human exposure. Exposure was from birth to adulthood (postnatal day 1 – 180) in parous and nulliparous rats.

2020-04-28 | GSE95554 | GEO

Diesel exhaust particle (DEP)-treated HBE cells

Project description:We evaluated the profile of lncRNA and mRNA expression in control and 50Î¼g/ml DEP treated HBE cells using the Arraystar Human LncRNA Array v3.0 array,7th generation. Our findings implicates that dysregulation of mitochondria invovled mRNAs may play important role in cytotoxicity of DEP. Examination of lncRNA and mRNA expression in control or DEP-treated HBE cells

2016-06-30 | E-GEOD-82335 | biostudies-arrayexpress

Diesel exhaust particle (DEP)-treated HBE cells

Project description:We evaluated the profile of lncRNA and mRNA expression in control and 50μg/ml DEP treated HBE cells using the Arraystar Human LncRNA Array v3.0 array,7th generation. Our findings implicates that dysregulation of mitochondria invovled mRNAs may play important role in cytotoxicity of DEP.

2016-06-30 | GSE82335 | GEO

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