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EC number: 200-554-5 | CAS number: 63-05-8
- 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
Additional toxicological data
Administrative data
- Endpoint:
- additional toxicological information
- Type of information:
- experimental study
- Adequacy of study:
- other information
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: published data
Data source
Referenceopen allclose all
- Reference Type:
- publication
- Title:
- Validation of an in vitro model for assessment of androstenedione hepatotoxicity using the rat liver cell line clone-9
- Author:
- Sahu SC et.al.
- Year:
- 2 008
- Bibliographic source:
- J. of Applied Toxicol. 28, 703-709
- Reference Type:
- publication
- Title:
- Effects of oral androstenedione on phospholipid fatty acids, ATP, caspase-3, prostaglandin E2 and C-reactive protein in serum and livers of pregnant and non-pregnant female rats
- Author:
- Wiesenfeld PW et.al.
- Year:
- 2 006
- Bibliographic source:
- Food and Chemical Toxicology 44, 579¿587
- Reference Type:
- publication
- Title:
- Effects of oral androstenedione on steroid metabolism in liver of pregnant and non-pregnant female rats
- Author:
- Flynn TJ et.al.
- Year:
- 2 005
- Bibliographic source:
- Food and Chemical Toxicology 43, 537¿542
- Reference Type:
- publication
- Title:
- Hepatotoxicity of androstenedione in pregnant rats
- Author:
- Sahu SC et.al.
- Year:
- 2 005
- Bibliographic source:
- Food and Chemical Toxicol. 43, 341-344
Materials and methods
Test material
- Reference substance name:
- Androst-4-ene-3,17-dione
- EC Number:
- 200-554-5
- EC Name:
- Androst-4-ene-3,17-dione
- Cas Number:
- 63-05-8
- Molecular formula:
- C19H26O2
- IUPAC Name:
- androst-4-ene-3,17-dione
Constituent 1
Results and discussion
Any other information on results incl. tables
Effects of androstendione on liver studied.
Applicant's summary and conclusion
- Executive summary:
In several publications, hepatotoxicity of Androstendione in vitro and in vivo was evaluated.
In an in vitro study, cultures of Clone-9 cells (non-transformed epithelial cell line that was originally
isolated from normal liver of a 4-week old Sprague-Dawley rat) were treated with androstenedione for 24 h at concentrations of 0-100 µg/ml. After the treatment period, the cells and the culture supernatants were assayed for markers of cytotoxicity which included: release of liver enzymes, cell viability, cellular double-stranded DNA content, oxidative stress, steatosis, cellular ATP content, caspase-3 activity, the mitochondrial permeability transition and induction of cytochrome P450 activity.
Significant concentration-dependent differences from control were observed in some endpoints (especially cell death and oxidative stress markers) at medium concentrations of 10 μg/ml and above. However, poor concordance between the hepatotoxicity of androstenedione in vitro in clone-9 cells and the hepatotoxicity of androstenedione in rats in vivo was observed, suggesting that the clone-9 cells are not a good model for predicting the hepatotoxicity of naturally occurring steroids (Sahu, 2008).
Mature female rats were gavaged with 0, 5, 30 or 60 mg/kg/day androstenedione beginning two weeks prior to mating and continuing through gestation day 19. Non-pregnant female rats were gavaged over the same time frame with 0 or 60 mg/kg/day androstenedione. Livers were removed from dams on gestation day 20 and from non-pregnant rats after five weeks_ treatment. Liver microsomes were incubated with 200 µM testosterone, and the reaction products were isolated and analyzed by HPLC. In pregnant rats, formation of 6a-, 15b-, 7a-, 16b-, and 2b-hydroxytestosterone was increased significantly vs. control at the highest dose level only. Formation of 6b-hydroxytestosterone increased significantly at both the 30 and 60 mg/kg/day dose levels. In non-pregnant rats, 60 mg/kg/day androstenedione significantly increased formation of 15b-, 6b-, 6b-, and 2b-hydroxytestosterone.
The data suggest that high oral doses of androstenedione can induce some female rat liver cytochromes P450 that metabolize steroid hormones and that the response to androstenedione does not differ between pregnant and non-pregnant female rats (Flynn, 2005).
Mature female rats were gavaged with 0, 5, 30 or 60 mg/kg/day androstenedione beginning two weeks prior to mating and continuing through gestation day 19. Non-pregnant female rats were gavaged over the same time frame with 0 or 60 mg/kg/day androstenedione. Serum was collected and livers were removed from dams on gestation day 20 and from non-pregnant rats after 5 weeks of treatment. Androstenedione had no effect on serum total cholesterol, triglycerides or HDL-cholesterol, but significantly decreased C-reactive protein in pregnant rats and prostaglandin E2 in serum of both pregnant and non-pregnant rats. There were treatment related decreases in liver ATP and, to a lesser degree, caspase-3 and no change in alkaline phosphatase of pregnant female rats. Androstenedione decreased docosahexaenoic acid in both serum and liver phospholipids of pregnant female rats. In conclusion, oral androstenedione did not result in overt hepatotoxicity in pregnant female rats, but produced modest changes in lipid metabolism and may impair regeneration of injured hepatic cells or tissue (Wiesenfeld, 2006).
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