Registration Dossier

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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Administrative data

Endpoint:
toxicity to reproduction: other studies
Type of information:
other: publication
Adequacy of study:
disregarded due to major methodological deficiencies
Reliability:
4 (not assignable)
Rationale for reliability incl. deficiencies:
other: secondary literature, no details

Data source

Reference
Reference Type:
publication
Title:
Unnamed
Year:
1991

Materials and methods

Principles of method if other than guideline:
no data
GLP compliance:
not specified
Type of method:
in vivo

Test material

Constituent 1
Chemical structure
Reference substance name:
4-vinylcyclohexene
EC Number:
202-848-9
EC Name:
4-vinylcyclohexene
Cas Number:
100-40-3
Molecular formula:
C8H12
IUPAC Name:
4-ethenylcyclohex-1-ene
Details on test material:
no data

Test animals

Species:
other: mouse and rat
Strain:
other: B6C3F1 mice and F344 rats
Sex:
female
Details on test animals or test system and environmental conditions:
no data

Administration / exposure

Route of administration:
intraperitoneal
Vehicle:
not specified
Analytical verification of doses or concentrations:
not specified
Details on analytical verification of doses or concentrations:
no data
Duration of treatment / exposure:
30 days
Frequency of treatment:
daily
Duration of test:
no data
Doses / concentrations
Remarks:
Doses / Concentrations:
10-800 mg/kg/day
Basis:
no data
No. of animals per sex per dose:
no data
Details on study design:
VCH and epoxide metabolites injected; some animals pretreated with chloramphenicol or phenobarbital
Statistics:
no data

Results and discussion

Observed effects

-mice:epoxides5-10 times more potent ovotoxins than VCH and in rats
-rats: 30 daily i.p. injections (800 mg/kg) of VCH failed to cause detectable ovotoxicity
-mice pretreated with chloramphenicol:69% inhibition of VCH epoxidation and protected mice from ovotoxocity.
- VCH epoxidation increased in phenobarbital pre-treated mice
-increasing VCH dose led to increase of circulating VCH epoxide (mice)

Applicant's summary and conclusion

Conclusions:
-VCH diepoxide is the most potent ovotoxic substance
- lack of ovotoxicity in VCH treated rats compared to mice because of slower rates of VCH biotransformation to epoxides and because of 20 fold higher rate of epoxide detoxification
- female B6C3F1 mouse : expression of P450IIA and P450IIB; female F344 rat: lack of related P450IIA mouse isoform and very low amounts of P450IIB