Bis(2-ethylhexyl) phthalate
(Synonyms: 邻苯二甲酸二(2-乙基己)酯,Bis(2-ethylhexyl) phthalate; Ergoplast FDO; ESBO-D 82) 目录号 : GC38654Bis(2-ethylhexyl) phthalate (Dioctyl phthalate, DOP, Diplast O, ESBO-D 82, Ergoplast FDO, Ergoplast FDO-S, Etalon) induces DNA strand breaks and gene expression alterations in larval zebrafish Danio rerio.
Cas No.:117-81-7
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Bis(2-ethylhexyl) phthalate (Dioctyl phthalate, DOP, Diplast O, ESBO-D 82, Ergoplast FDO, Ergoplast FDO-S, Etalon) induces DNA strand breaks and gene expression alterations in larval zebrafish Danio rerio.
[1] Halis Boran, Serap Terzi. Toxicol Ind Health. 2019 Aug;35(8):520-529.
Cas No. | 117-81-7 | SDF | |
别名 | 邻苯二甲酸二(2-乙基己)酯,Bis(2-ethylhexyl) phthalate; Ergoplast FDO; ESBO-D 82 | ||
Canonical SMILES | O=C(C1=CC=CC=C1C(OCC(CC)CCCC)=O)OCC(CC)CCCC | ||
分子式 | C24H38O4 | 分子量 | 390.56 |
溶解度 | DMSO: 150 mg/mL (384.06 mM) | 储存条件 | Store at -20°C, protect from light |
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1 mM | 2.5604 mL | 12.8021 mL | 25.6043 mL |
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10 mM | 0.256 mL | 1.2802 mL | 2.5604 mL |
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Applying the adverse outcome pathway concept for assessing non-monotonic dose responses: biphasic effect of Bis(2-ethylhexyl) phthalate (DEHP) on testosterone levels
Arch Toxicol 2023 Feb;97(2):313-327.PMID:36336711DOI:10.1007/s00204-022-03409-9.
Male reproduction is one of the primary health endpoints identified in rodent studies for some phthalates, such as DEHP (Bis(2-ethylhexyl) phthalate), DBP (Dibutyl phthalate), and BBP (Benzyl butyl phthalate). The reduction in testosterone level was used as an intermediate key event for grouping some phthalates and to establish a reference point for risk assessment. Phthalates, and specifically DEHP, are one of the chemicals for which the greatest number of non-monotonic dose responses (NMDRs) are observed. These NMDRs cover different endpoints and situations, often including testosterone levels. The presence of NMDR has been the subject of some debate within the area of chemical risk assessment, which is traditionally anchored around driving health-based guidance values for apical endpoints that typically follow a clear monotonic dose-response. The consequence of NMDR for chemical risk assessment has recently received considerable attention amongst regulatory agencies, which confirmed its relevance particularly for receptor-mediated effects. The present review explores the relationship between DEHP exposure and testosterone levels, investigating the biological plausibility of the observed NMDRs. The Adverse Outcome Pathway (AOP) concept is applied to integrate NMDRs into Key Event Relationships (KERs) for exploring a mechanistic understanding of initial key events and possibly associated reproductive and non-reproductive adverse outcomes.
Ingestion of Bis(2-ethylhexyl) phthalate (DEHP) during adolescence causes depressive-like behaviors through hypoactive glutamatergic signaling in the medial prefrontal cortex
Environ Pollut 2021 Nov 15;289:117978.PMID:34426190DOI:10.1016/j.envpol.2021.117978.
Over the past decades, the production and use of hazardous chemicals has increased worldwide, and the incidence of neurological diseases is increasing proportionately. Among these chemicals, Bis(2-ethylhexyl) phthalate (DEHP) is the most common member of the phthalate family used as a plasticizer. The present study assessed the consequences of daily DEHP ingestion and its effects on brain functions related to depressive-like behaviors. Adolescent C57BL/6 male mice ingested different concentrations of DEHP in their diet (2, 20, and 200 mg/kg of diet), and behavioral changes in anxiety, despair, anhedonia, and sociality were investigated. DEHP exposure evoked depressive-like behaviors in a dose-dependent manner for each symptom. The levels of corticosterone and reactive oxygen species/reactive nitrogen species increased in DEHP-exposed groups, suggesting chronic stress-like responses. In the medial prefrontal cortex (mPFC), glutamate and glutamine were decreased, and glutamine synthetase showed lower activity compared to the control group, suggesting imbalanced glutamatergic signaling. Measuring the spontaneous excitatory postsynaptic current of glutamatergic neurons, we found that DEHP ingestion resulted in hypoactive glutamatergic signaling in the mPFC.
Bis(2-ethylhexyl) phthalate induces DNA strand breaks and gene expression alterations in larval zebrafish Danio rerio
Toxicol Ind Health 2019 Aug;35(8):520-529.PMID:31462198DOI:10.1177/0748233719869531.
Contamination of the aquatic environment by plastic industrial products and their by-products is remarkable. Because of their physical, chemical, and biological degradation resistance, plasticizers can enter the food chain of living organisms, accumulate in the body and generate toxic effects. Here we determined the potential toxic effects of Bis(2-ethylhexyl) phthalate (DEHP) plasticizer to larval (72 h post fertilization) zebrafish (Danio rerio) by analyzing changes in expression levels of stress-related genes (p53, rad51, and xrcc5) by the quantitative real-time polymerase chain reaction. Also, possible DNA damage by DEHP in larvae was determined. The concentration of DEHP (0-160 mg/l) that killed 50% of the larval zebrafish within 96 h was 54.02 mg/l. There was a concentration-related increase in DNA damage in cells from larvae exposed (96 h) to DEHP. DNA damage of 31.13% (mean ± standard error of the mean) was observed in larvae at the highest sublethal DEHP concentration (10 mg/l). Some significant differences in the induction of stress-related genes were also observed in larvae exposed to DEHP relative to control (p < 0.05). The conclusion drawn from this ecotoxicological risk assessment is that, under present use and exposure patterns, DEHP presents a small hazard to zebrafish larvae.
Quantification of Bis(2-ethylhexyl) phthalate released by medical devices during respiratory assistance and estimation of patient exposure
Chemosphere 2020 Sep;255:126978.PMID:32417514DOI:10.1016/j.chemosphere.2020.126978.
Bis(2-ethylhexyl) phthalate (DEHP) migration from polyvinyl chloride (PVC) has been studied with infusion, transfusion and extracorporeal oxygenation devices, but no study has been conducted to estimate its migration via respiratory medical devices (MDs). This work aims to develop an ex vivo model to quantify DEHP released doses by these MDs, which will then be used to estimate newborns DEHP exposure from respiratory assistance MDs. We followed the Frensh National Research and Safety Institute (INRS) recommendations for the validation of a collecting and analysing method of DEHP in air, which will be used to quantify DEHP in air passing through PVC respiratory assistance MDs. The developed method met all the validation criteria for DEHP determination in air. DEHP in air passing through MDs on the sixth day reached a cumulative quantity of 122.86 μg when using a flow rate of 4 L min-1 of non-humidified air while it was of 49.22 μg; 58.12 μg and 29.61 μg with flow rates of 2 L min-1 of humidified air, 2 L min-1 of dry air and 4 L min-1 of humidified air, respectively. Model application to two patients undergoing two different respiratory procedure demonstrated that noninvasive ventilation patient received higher dose of inhaled DEHP, confirmed by DEHP metabolites quantification in urine. Although the protective effect of air humidifiers on DEHP exposure was demonstrated, the effect of flow rate is difficult to be established. This developed method should be tested to verify its capacity to collect and quantify other plasticizers used in PVC MDs.
Degradation of Bis(2-ethylhexyl) phthalate constituents under methanogenic conditions
Biodegradation 1996;7(6):501-6.PMID:9188196DOI:10.1007/BF00115296.
The degradation of Bis(2-ethylhexyl) phthalate (DEHP) and its intermediary hydrolysis products 2-ethylhexanol (2-EH) and mono(2-ethylhexyl) phthalate (MEHP) was investigated in a methanogenic phthalic acid ester-degrading enrichment culture at 37 degrees C. 2-Ethylhexanoic acid (2-EHA), a plausible degradation product of 2-EH, was also studied. The culture readily degraded 2-EH via 2-EHA to methane which was formed in stoichiometric amounts assuming complete degradation of 2-EH to methane and carbon dioxide. MEHP was degraded to stoichiometric amounts of methane with phthalic acid as a transient intermediate. DEHP remained unaffected throughout the experimental period (330 days).