ArticleInternational journal of environmental research and public health2019
The Increase of ROS Caused by the Interference of DEHP with JNK/p38/p53 Pathway as the Reason for Hepatotoxicity.
Article in International journal of environmental research and public health, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- The potential mechanisms underlying phthalate-induced hypospadias: a systematic review of rodent model studies.Frontiers in endocrinology · 2024Pooled it
- DEHP induces stress urinary incontinence by causing urethral sphincter dysfunction via inflammation and apoptosis: a mechanism study based on animal experiments, network toxicology, and molecular docking.Frontiers in cell and developmental biology · 2026Article
- Molecular Mechanisms of Phthalate-Induced Hepatic Injury and Amelioration by Plant-Based Principles.Toxics · 2025Review
- Phthalates and epigenetics: An emerging public health concern.Current research in toxicology · 2025Review
- Hierarchical plant extracts in silver nanoparticles preparation: Minuscular survey to achieve enhanced bioactivities.Heliyon · 2024Article
- Phthalate exposure induces cell death and ferroptosis in neonatal microglial cells.Turkish journal of medical sciences · 2024Article
- Preconception and developmental DEHP exposure alter liver metabolism in a sex-dependent manner in adult mouse offspring.Toxicology · 2023Article
- Article
- Di-(2-ethylhexyl) Phthalate Limits the Lipid-Lowering Effects of Simvastatin by Promoting Protein Degradation of Low-Density Lipoprotein Receptor: Role of PPARγ-PCSK9 and LXRα-IDOL Signaling Pathways.Antioxidants (Basel, Switzerland) · 2023Article
- Dimethyl Fumarate Attenuates Di-(2-Ethylhexyl) Phthalate-Induced Nephrotoxicity Through the Nrf2/HO-1 and NF-κB Signaling Pathways.Inflammation · 2023Article
- Article
- Protective effect of Lycium barbarum polysaccharide on di-(2-ethylhexyl) phthalate-induced toxicity in rat liver.Environmental science and pollution research international · 2021Article
- Prediction and mechanistic analysis of drug-induced liver injury (DILI) based on chemical structure.Biology direct · 2021Article
- Di-(2-ethylhexyl) phthalate-induced tumor growth is regulated by primary cilium formation via the axis of HInternational journal of medical sciences · 2021Article
- Oxidative damage, inflammation, genotoxic effect, and global DNA methylation caused by inhalation of formaldehyde and the purpose of melatonin.Toxicology research · 2020Article
- Multi and transgenerational epigenetic effects of di-(2-ethylhexyl) phthalate (DEHP) in liver.Toxicology and applied pharmacology · 2020Article
- [Effects of Shoutai pills on immune function and oxidative stress in pregnant rats with di(2-ethylhexyl) phthalate exposure].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- The Impact of Di-2-Ethylhexyl Phthalate on Sperm Fertility.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As the most commonly used plasticizer, Di-(2-ethylhexyl)-phthalate (DEHP) exists everywhere in the environment due to the widespread use of polyvinyl chloride (PVC) in human life, and it is also a recognized environmental pollutant. Studies have proved the hepatotoxicity of DEHP, however the mechanism has not been adequately explored, especially the role of the reactive oxygen species (ROS) in it. In the present study, 21 day-old ICR mice were administered DEHP with dose of 0, 125, 250, and 375 mg/kg/day for 28 days by intragastrical gavage. After contamination, histopathology displayed that liver tissue were damaged mildly with the effect of DEHP; a significant increase of the serum liver function index (including aspartate transaminase (AST) and alanine transaminase (ALT)) were observed. Additionally, the level of lipid peroxidation markedly rise, especially ROS and malondialdehyde (MDA), but the activation of superoxide dismutase (SOD) was obviously decreased in mice liver. In addition, DEHP promoted the phosphorylation of JNK and p38MAPK proteins in mice liver, as well as increased the expression of p53 protein and decreased the level of DNA methylation in the p53 gene promoter region. These results indicated that the hepatotoxicity of mice caused by DEHP may be through activating the JNK/p38MAPK/p53 signaling pathway and further promoting the generation of ROS to induce lipid peroxidation in liver, and the role of DNA methylation may be inevitable.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.