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Updated: Aug 16, 2026
Transgenic Rodent Assay for Quantifying Male Germ Cell Mutant Frequency
Published on: August 6, 2014
Induction of dominant lethal mutations in male mice by fosfestrol
Abstract:
Using the dominant lethal assay, the ability of fosfestrol, a diethylstilboestrol derivate, to induce mutations in male mice was tested and confirmed. Up to 300 mg/kg of fosfestrol the induction of mutations occurs exclusively in spermatozoa. A dose of 600 mg/kg of fosfestrol induces dominant lethal mutations up to 10 days posttreatment. The majority of induced dominant lethal mutations in all dose groups are expressed as loss after implantation.
Insights
Fosfestrol, a diethylstilbestrol derivative, was confirmed to induce mutations in male mice. Higher doses caused mutations primarily in spermatozoa, leading to post-implantation losses.
Area of Science:
- Toxicology
- Genetics
- Reproductive Toxicology
Background:
- Diethylstilbestrol derivatives are investigated for potential genotoxic effects.
- Understanding the mutagenic potential of fosfestrol is crucial for risk assessment.
Purpose of the Study:
- To evaluate the mutagenic capacity of fosfestrol in male mice using the dominant lethal assay.
- To determine the dose-response relationship and the stage of germ cell mutation induction.
Main Methods:
- The dominant lethal assay was employed in male mice.
- Mice were treated with varying doses of fosfestrol (up to 600 mg/kg).
- Mutations were assessed through post-implantation loss analysis.
Main Results:
- Fosfestrol induced dominant lethal mutations in male mice.
- At doses up to 300 mg/kg, mutations were observed exclusively in spermatozoa.
- A dose of 600 mg/kg induced mutations up to 10 days post-treatment.
- The majority of mutations resulted in post-implantation losses.
Conclusions:
- Fosfestrol exhibits mutagenic activity in male mice.
- Spermatozoa are a primary target for fosfestrol-induced mutations.
- The dominant lethal assay effectively detected fosfestrol's genotoxicity, primarily manifesting as early embryonic lethality.
