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Diss Factsheets
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EC number: 700-342-7 | CAS number: 1163775-81-2
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
![](https://www.echa.europa.eu/o/diss-blank-theme/images/factsheets/A-REACH/factsheet/print_toxicological-information.png)
Specific investigations: other studies
Administrative data
- Endpoint:
- toxicogenomics
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
- Study period:
- 2010
- Reliability:
- 2 (reliable with restrictions)
Data source
Reference
- Reference Type:
- study report
- Title:
- Unnamed
- Year:
- 2 010
Materials and methods
- Principles of method if other than guideline:
- To assess the potential to induce testicular mal-development (TMD) in the rat by studying effets on the expression of genes in pathways known to be involved in steroidogenesis and testes development that have previously been shown to be involved in the induction of TMD.
- GLP compliance:
- no
- Type of method:
- in vivo
- Endpoint addressed:
- developmental toxicity / teratogenicity
Test material
- Reference substance name:
- 1,2,4-Benzenetricarboxylic acid, decyl octyl ester
- EC Number:
- 268-007-3
- EC Name:
- 1,2,4-Benzenetricarboxylic acid, decyl octyl ester
- Cas Number:
- 67989-23-5
- Molecular formula:
- not applicable, UVCB
- IUPAC Name:
- 1,2,4-Benzenetricarboxylic acid, decyl octyl ester
- Test material form:
- liquid
- Details on test material:
- - Name of test material (as cited in study report): 1,2,4-Benzentricarboxylic acid, decyl octyl ester, Label name LINPLAST 810 TM unstab.
- Substance type: pure active substance
- Physical state: liquid
- Stability under test conditions: no data
- Storage condition of test material: ambient temperature
Constituent 1
- Specific details on test material used for the study:
- N/A
Test animals
- Species:
- rat
- Strain:
- other: Han Wistar
- Sex:
- male/female
- Details on test animals or test system and environmental conditions:
- 24 female and 5 male Han Wistar rats (10-12 weeks old) were housed 3 per cage on sawdust in solid-bottom, polypropylene cages. The rats were acclimatised for at least 5 days before use. In the animal room, the environment was controlled to provide conditions suitable for the Wistar strain of rat.The temperature was maintained within a range of 19-23 deg C and relative humidity within a range of 40-70%. There were, nominally, 14-15 air changes per hour. Twelve-hour periods of light were cycled with twelve-hour periods of darkness.
Administration / exposure
- Route of administration:
- oral: gavage
- Vehicle:
- corn oil
- Details on exposure:
- Pregnant dams were treated daily with vehicle (corn oil) or L810TM by oral gavage on gestation days 12 to 19 inclusive. Di(2-ethylhexyl) phthalate (DEHP) was used as a positive control.
- Analytical verification of doses or concentrations:
- no
- Details on analytical verification of doses or concentrations:
- N/A
- Duration of treatment / exposure:
- Gestation days 12 to 19 inclusively
- Frequency of treatment:
- Daily
- Post exposure period:
- Dams were killed on gestation day 19 and foetuses removed.
Doses / concentrations
- Remarks:
- Doses / Concentrations:
500 mg/kg
Basis:
nominal conc.
- No. of animals per sex per dose:
- Testes from a minimum of 5 litters per treatment group
- Control animals:
- yes, concurrent vehicle
- Details on study design:
- Male rats were exposed in¿utero by oral gavage of the dam and transcriptional profiling analysis of RNA extracted from neonatal testes was used to gain insight into the potential effects on pathways relevant to testicular mal-development (TMD). Male and female animals were randomly selected for mating. Owing to the propensity of rat vaginal plugs to drop out following mating, there was a need to mate animals one on one in wire bottom cages, so as to be able to confirm that mating had occurred and for the selection of time-mated females. Time-mated females were treated from gestation day (GD) 12-19 inclusive with either vehicle (corn oil) DEHP or L810TM (500 mg/Kg) by oral gavage all at a dose volume of 1 mL/Kg. On GD 19, dams were killed by inhalation of an increasing concentration of carbon dioxide. Foetuses were removed and killed by decapitation. Foetal gonads were dissected using a dissecting microscope. Testes from a minimum of 5 litters per treatment group were micro-dissected and snap frozen in liquid nitrogen. Pairs of snap frozen testes, two from each pup, were stored at -80°C prior to RNA isolation for microarray analysis and possible LCMS analysis.
Pools of foetal testes from a minimum of three pups per litter (6 foetal testes) were disrupted using a qiashredder column and purified using RNeasy mini columns according to the CXR method entitled `Method for Isolation of RNA from Foetal Rat Testes for use in Microarray Analysis¿ (Plummer et al, 2007). RNA integrity was checked using the Agilent Bioanalyser and the RNA nano or pico Lab chip kit according to the Agilent protocol entitled `RNA 6000 Nano/Pico Assay¿. Total RNA (100ng-1mg) was labelled prior to microarray hybridisation using the Agilent Quick Amp Labelling Kit One Colour (Agilent# 5190-0442). Agilent 4x44K Whole Rat Genome Oligo Microarray slides (G4131F) were hybridised, washed and then scanned on an Agilent Microarray Scanner.
Images from the scanner were processed using Agilent Feature Extraction Software v9.1. Rosetta ResolverTM 6 software was used to define a list of significantly altered genes (the ¿Signature List¿). Signature lists of significantly (p<0.01) altered genes were filtered to remove low intensity genes.
Bioinformatic analysis using Ingenuity Pathways AnalysisTM (IPA) software was used to identify genes in the signature lists that are associated with the TMD target pathways of testosterone synthesis and cryptorchidism. Lists of genes in these pathways relevant to TMD were constructed using from data derived from previous transcriptional profiling studies (Liu et al. 2005; Plummer et al. 2007).
Examinations
- Examinations:
- Changes in gene expression in pathways relevant to TMD, (e.g steroidogenesis, cholesterol metabolism and transport and guvernacular ligament development), by transcription profiling analysis of RNA.
- Positive control:
- Di(2-ethylhexyl) phthalate (DEHP), at a dose of 500 mg/kg, was used as a positive control.
Results and discussion
- Details on results:
- 564 and 3406 gene expression changes (P<0.01), relative to control, were caused by DEHP (500mg/Kg) and L810TM, respectively.
From a toxicological point of view, it is more relevant to analyze the effects of compounds in the context of functional pathways rather than looking at individual genes. Hence, analysis of all the signature gene expression changes (>1.5 fold) in the IPA database against gene/pathway information. Representation analysis of bias towards effects on particular pathways in the gene lists relative to the IPA database, identified pathways (1-7) that were significantly over-represented in the DEHP and TOTM gene lists. DEHP treatment caused bias towards effetcs in the pathways of steroidogenesis and steroid metabolism. Genes in this pathway, namely 3-hydroxy 3-methylglutaryl-Coenzyme A reductase (HMGCR), cytochrome P450 short chain cleavage (CYP11A), cytochrome P450 17 alpha-hydroxylase (CYP17A), steroidogenic acute regulatory protein (STAR), delta(5)-3-beta, hydroxysteroid dehydrogenase-1 (HSD3B1) and sterol isomerase (EBP), were down-regulated.
By contrast, the L810TM signature gene list showed a bias towards effects on the pathways of hepatic stellate cell activation, glucocorticoid signalling, integrin signalling, androgen signalling and MAPK signalling. None of these effects were considered to be relevant to TMD.
To compare the effects of the different treatments on genes responsible for the testosterone hormone synthesis, the data from the gene lists were superimposed on a TMD pathway derived from previous mechanistic studies on certain phthalates (CXR0206, CXR0409), (Plummer et al. 2007). In the present study, the results showed that DEHP caused a repression of genes involved in testes development and cholesterol and testosterone biosynthesis.
L810TM had no significant repressive effect on genes in the TMD pathway,
Any other information on results incl. tables
N/A
Applicant's summary and conclusion
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.
Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
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