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Clastogenicity of tritiated thymidine to the mouse bone marrow
Abstract:
Tritiated thymidine (3HTdR; 120 microCi/mouse) increases the incidence of micronucleated polychromatic erythrocytes (MPE) in bone marrow PE of both B6CF1 and CBA male mice. This effect observed in vivo reflects, the clastogenicity reported by other investigators for 3HTdR in vitro. Thymidine itself was concluded to be inactive in the assay at a dose-level 100 times greater than that required to show activity for 3HTdR. These observations are of relevance to those employing 3HTdR to monitor the mitogenic activity and the genotoxicity of chemicals.
Insights
Tritiated thymidine (3HTdR) increases micronucleated polychromatic erythrocytes (MPE) in mice, indicating genotoxicity. Thymidine alone showed no such effect, highlighting 3HTdR
Area of Science:
- Toxicology
- Genetics
- Biochemistry
Background:
- Tritiated thymidine (3HTdR) is used to assess cellular proliferation and genotoxicity.
- Previous in vitro studies suggest 3HTdR exhibits clastogenic effects.
Purpose of the Study:
- To evaluate the in vivo genotoxic potential of tritiated thymidine (3HTdR).
- To compare the effects of 3HTdR with unlabeled thymidine in a mouse model.
Main Methods:
- Administration of 3HTdR to male B6CF1 and CBA mice.
- Analysis of micronucleated polychromatic erythrocytes (MPE) in bone marrow.
- Dose-response assessment comparing 3HTdR and thymidine.
Main Results:
- 3HTdR significantly increased the incidence of MPE in both mouse strains.
- Unlabeled thymidine did not induce MPE even at high doses.
- The in vivo findings corroborate in vitro clastogenicity data for 3HTdR.
Conclusions:
- 3HTdR is confirmed to be genotoxic in vivo, causing chromosomal damage.
- Thymidine itself is not genotoxic under the tested conditions.
- These findings are crucial for interpreting studies using 3HTdR for mitogenic and genotoxic assessments.