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PubMedDate not supplied

Di-2-ethylhexyl phthalate (DEHP) and mono-2-ethylhexyl phthalate (MEHP) accumulation in whole blood and red cell concentrates.

Plasma DEHP concentrations were measured weekly in whole blood and red cell concentrates (RCC) during 21 days of storage in standard CPD within PL-130 blood bags. In addition, DEHP and MEHP accumulation patterns were investigated in blood stored for 42 days in modified CPD with adenine within PL-146 and BB-69 storage containers. Total per-unit plasma DEHP of RCC units was 49 to 71 per cent of the total in plasma of whole blood units (PL-130). From 28 to 42 days, mean DEHP levels were 12 to 19 per cent higher in whole blood stored in PL-146 than in BB-69. Although MEHP was not found in any blood bag plastic, MEHP accumulated in plasma during whole blood storage. MEHP concentrations were 2.8 to 3.8 times higher in plasma stored in BB-69 than in PL-146. It is postulated that MEHP arises from hydrolysis of DEHP by plasma lipase, even in frozen plasma sample, and that the rate of this reaction is influenced by blood bag plastic surface characteristics.

Blood Preservation↗
PubMed1978

Effect of Di-(2-ethylhexyl) phthalate (DEHP) on chemical constituents and enzymatic activity of rat liver.

Effect of Di(2-ethylhexyl) phthalate (DEHP), was investigated on chemical constituents and activity of certain enzymes of rat liver. A significant increase in liver weight; total and relative to body weight; decrease in total, free and esterified cholesterol; and no change in dry weight, moisture; RNA, DNA, total lipids, phospholipids, pyruvic acid and lactic acid contents was observed in liver of DEHP-treated rats as compared to controls. Activity of 3 mitochondrial enzymes, malic dehydrogenase, cytochrome-c-oxidase and diaphorase were significantly decreased while that of NADH-cytochrome c reductase, RNAase and DNAase remained unaltered upon treatment. The results suggest that DEHP exerts its hepatotoxic effects by interfering with bioenergetics of the cell.

Animals↗
PubMed1978

Di-2-ethylhexylphthalate (DEHP) content of blood or blood components stored in plastic bags.

Di-2-ethylhexylphthalate (DEHP) is a plasticizer used in the manufacture of plastic bags for blood products, which may be toxic. No more than a trace (less than 0.1 microgram/ml) could be detected in anticoagulants in blood bags, or in the blood of healthy untransfused subjects. A mean of 23 microgram/ml was found in ACD whole blood after 2 weeks storage, and 46 microgram/ml after 3 weeks; the corresponding figures for packed cells were 39 and 45 microgram/ml. The level in CPD whole blood was similar. Fresh frozen plasma and cryoprecipitate contained 7 microgram/ml, while levels of 1.0 and 0.7 microgram/ml of DEHP were found in the blood of two patients who had received massive transfusions. Most DEHP in stored blood was associated with plasma lipoproteins.

Anticoagulants↗
PubMedDate not supplied

DEHP in blood.

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Diethylhexyl Phthalate↗
PubMed2026

Elevated phthalate exposure and metabolic susceptibility increased breast cancer risk: A 20-y follow-up study in Taiwan.

Widely used phthalates, especially di-(2-ethylhexyl) phthalate (DEHP), increase breast cancer risk in experimental animals and humans, but long-term follow-up evidence of its human breast carcinogenicity remains inconclusive. This nested case-control study included 119 invasive breast cancer cases and 245 matched controls from a longitudinal cohort of 11,923 women recruited in 1991-1992 and followed to 2010 in Taiwan. Urine samples at baseline and follow-up visit were tested for 11 metabolites of seven phthalates using LC-ESI-MS/MS. DEHP metabolism susceptibility was evaluated by the percentage of mono-2-ethylhexyl phthalate (MEHP%) in the sum of five DEHP metabolites (∑DEHP). Odds ratios (ORs) with 95% CI from conditional logistic regression were used to examine risk predictors. DEHP was the only phthalate significantly associated with breast cancer risk. Risk increased significantly with elevated urinary levels of ∑DEHP (> 0.381 μmol/g creatinine, OR = 1.71, 95% CI = 1.02 to 2.43), MEHP (> 0.022 μmol/g creatinine, OR = 1.87, 95% CI = 1.07 to 3.25), and MEHP% (> 6.7%, OR = 1.65, 95% CI = 0.96 to 2.82). Elevated ∑DEHP and MEHP% combined with early menarche (≤ 14 years) was associated with further increased risk (OR = 7.52, 95% CI = 2.68 to 21.05). The intraclass correlation coefficient between paired baseline and follow-up samples of 152 women was 0.06 for ∑DEHP and 0.31 for MEHP%. High DEHP exposure, high MEHP%, and early menarche were associated with increased breast cancer risk. MEHP% was a better biomarker for DEHP metabolism.

Humans↗
PubMed2026

Screening of core targets for Di(2-ethylhexyl) Phthalate-related gastric cancer based on machine learning, molecular docking, and SHAP analysis.

PURPOSE: Given the existing uncertainties regarding the link between Di(2-ethylhexyl) phthalate (DEHP) exposure and gastric cancer (GC) progression, this study aimed to clarify their association, identify the toxic targets of DEHP, and elucidate the underlying molecular mechanisms. METHODS: Multiple integrated approaches were employed, including Gene Expression Omnibus (GEO) data analysis, network toxicology, molecular docking, and machine learning. STRING and Cytoscape tools were utilized to identify key targets, while Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to explore the functional enrichment of intersecting targets. Machine learning and SHAP analysis were applied to screen core targets in GC. Molecular docking was performed to evaluate the binding affinity of DEHP toward core targets, and 200 ns molecular dynamics simulations were further conducted for representative complexes to validate their dynamic stability. RESULTS: A total of 18 key targets were identified using STRING and Cytoscape. GO and KEGG enrichment analyses demonstrated that these intersecting targets were primarily enriched in the extracellular region, as well as the Calcium signaling pathway and cAMP signaling pathway. Through machine learning analyses, 7 key genes (ADRB2, ESRRG, GRIA4, IL13RA2, NR3C2, PLA2G1B, and SULT2A1) were identified as core targets in GC through machine learning analyses. Molecular docking simulations revealed strong binding specificity between DEHP and the target proteins. Among them, NR3C2 and ADRB2 exhibited relatively high predictive importance in the machine learning models. DEHP showed favorable binding affinity toward these core targets, and molecular dynamics simulations further confirmed that ADRB2-DEHP and NR3C2-DEHP complexes maintained stable conformations throughout the simulation. CONCLUSIONS: Our findings identified GC associated genes that were computationally predicted as potential targets of DEHP. These results indicated structural compatibility between DEHP and its target proteins but did not prove that DEHP exposure accounts for the gene expression changes in GC.

Molecular Docking Simulation↗
PubMedDate not supplied

Tissue analysis of plasticizer in dogs.

Acute renal failure was produced in animals and analytical procedures for DEHP estimation in urine and tissues of dogs developed. The presence of DEHP in urine samples of control and sham operated dogs indicated that significant excretion of this plasticizer by kidney occurred. Delay in elevation of DEHP serum levels in nephrectomized dogs and similar concentrations of DEHP in 72 hr and 96 hr serum samples in all 3 groups indicate possible metabolism and/or uptake of DEHP by tissues. DEHP levels in brain, heart, and lung tissues of nephrectomized dogs were higher than those in control and sham operated dogs; however, the highest concentration of DEHP was found in lung regardless of grouping. Gas chromatographic spectra of kidney and liver homogenates showed several extraneous peaks with shorter retention times than DEHP, probably representing metabolites of DEHP. Identification and quantitation of DEHP metabolites in tissues are presently under way in our laboratory.

Acute Kidney Injury↗
PubMed2026

Analysis of the molecular mechanism underlying di(2-ethylhexyl) phthalate-induced bladder carcinogenesis via network toxicology and molecular docking approaches: An observational study.

This study aims to investigate the toxicity of di(2-ethylhexyl) phthalate (DEHP) and the potential molecular mechanisms of DEHP-induced bladder cancer (BLCA) using network toxicology and molecular docking strategies. The toxicity of DEHP was assessed using Prox-II software, and potential targets for DEHP-induced BLCA were identified by integrating data from ChEMBL database, Search Tool for Interactions of Chemicals, SwissTargetPrediction, GeneCards, Therapeutic Target Database, Online Mendelian Inheritance in Man, and The Cancer Genome Atlas. STRING database and Cytoscape were employed to construct target networks and determine core targets. The expression levels of core targets were analyzed using R. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed on potential and core targets. Molecular docking was carried out using CB-Dock 2 to verify the interactions between DEHP and core targets. A total of 105 potential targets related to DEHP-induced BLCA were identified, from which 7 core targets were selected: cyclin-dependent kinase 1, interleukin 6, cyclin-dependent kinase 2, cyclin B1, Erb-B2 receptor tyrosine kinase 2, cyclin B2, and B-cell lymphoma 2. IL-6 and B-cell lymphoma 2 showed downregulated expression in tumor tissues, while cyclin-dependent kinase 1, cyclin-dependent kinase 2, cyclin B1, Erb-B2 receptor tyrosine kinase 2, and cyclin B2 were upregulated. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses indicated that these targets were enriched in cell signaling and cancer-related pathways. Molecular docking confirmed that DEHP interacts with these core targets. DEHP may promote the development of BLCA by interacting with key proteins and signaling pathways. This study provides a theoretical basis for understanding the molecular mechanisms of DEHP-induced BLCA and offers references for future prevention and treatment strategies.

Diethylhexyl Phthalate↗
PubMedDate not supplied

[Toxicity of the PVC-plasticizer di(2-ethylhexyl)phthalate (author's transl)].

The plastizicer di(2-ethylhexyl)phthalate (DEHP) is produced in hundreds of thousands tons and has got a widespread use in a multitude of PVC-plast products. In the present review the toxicology and possible harmful environmental effects of DEHP is discussed. The four following topics have also been considered: 1. The solubility of DEHP in water and the complex between DEHP and fulvic acid. 2. Residues and metabolites of DEHP in fish and invertebrates. 3. The metabolites of DEHP in rat, where four major metabolites have been found (fig. 1). 4. The problem concerning residues of DEHP in blood stored in PVC plastic bags for transfusion and the relationship of DEHP to microaggregation of platelets in stored blood. Although the oral LD50 in the rat, mouse and rabbit is about 30 g/kg, its toxicology reveals problematic features such as high toxicity to some invertebrates, specific effects on the nervous system of fish and teratogenic effects in rats.

Animals↗
PubMed1978

Diethylhexyl phthalate as a factor in blood transfusion and haemodialysis.

Di-2-ethylhexyl phthalate (DEHP), the most frequently occurring plasticiser in medical equipment manufactured from polymers of vinyl chloride, forms about 40% w/w of tubes and containers used for storing blood and for haemodialysis. The plasticiser leaches out into liquids with lipid contents, although it is very sparingly soluble in purely aqueous solutions. On infusion of 2-3 1 of stored blood, up to 200 mg DEHP may be transferred to the patient, while much higher quantities may be given during dialysis, which is moreover often repeated frequently over long periods. The acute toxicity of DEHP is very low (greater than 20 g/kg as LD50 in rats), and the ester is rapidly metabolised to products which are excreted in the urine and bile; chronic toxicity from the levels of dosage obtaining is thus very improbable. Carcenogenicity has never been demonstrable in animals, while teratological effects are of a very low order. Serious acute results observed after transfusion of neonates have not been proved to be caused by DEHP, and might be ascribable to accompanying foreign substances. Atheroma in chronic dialysis subjects is still unexplained, but hepatitis probably caused by diethylphthalate from plastic was resolved when apparatus plasticised by DEHP alone was substituted. The benefits of DEHP appear vastly to outweigh any risks. The status of DEHP as environmental contaminant is noted.

Animals↗
PubMed1979

[Release of diethyl-2-hexyl phthalate from stored blood on contact with polyvinyl chloride].

Softness and flexibility of PVC are due to the addition of plasticizers in high concentration; the most used of them for blood storage bags is DEHP. In this work, a method for labelling DEHP with 14C from 14C phtalic anhydrid is given. A piece of PVC from a commercial blood bag is labelled, in our laboratory, with 14C DEHP and used to follow the kinetics of DEHP leaching in blood during storage. It is also used to study the influence of some parameters such as lipids amount of blood, shaking, and plastic sterilisation on this leaching. DEHP leaching is a three steps phenomenon and the level is not correlated to lipids content of blood. Thermal treatment of PVC and shaking have an influence on leaching. DEHP is not metabolised during blood storage at 4 degrees C and can not be detected as free molecule; it is absorbed on plasmatic proteins.

Blood Preservation↗
PubMed1978

Effects of di-(2-ethylhexyl)phthalate administration on carbohydrate and fatty acid metabolism in rat liver.

1. Rats were fed on a diet containing 0, 1, 2, or 4% di-(2-ethylhexyl)phthalate (DEHP), a widely used plasticizer, for four weeks. 2. The level of plasma triglyceride was decreased in both the 1% DEHP and the 2% DEHP groups maintained for 1 to 2 weeks, but that of cholesterol was not changed. Plasma free fatty acid and ketone bodies increased in all DEHP groups. 3. The level of blood glucose was depressed to about 80% in the 2% and the 4% DEHP groups. Liver glycogen decreased markedly. Isotopic incorporations of 14C from [2-14C]pyruvate into blood glucose and liver glycogen were decreased. The changes in the contents of intermediates in the liver indicate that gluconeogenesis is inhibited at the reaction(s) between 3-phosphoglycerate and fructose 1,6-diphosphate. 4. Hepatic fatty acid synthesis increased about 2-fold on DEHP administration. The content of phospholipid in the liver was increased, whereas that of triglyceride was decreased. The rate of phospholipid synthesis was increased, but that of triglyceride was not changed.

Acetates↗