Spontaneous and induced frequency of transplacental micronucleus in Balb/c m

2014 
Introduction : The transplacental micronuclei assay has been developed aimed at evaluating the genotoxic potential in the descendants, demonstrating the capacity of an agent for causing cromosomal damages during the prenatal period. The registration of the cromosomal aberrations shows when a specific substance may be clastogenic or aneugenic in the fetus through the maternal exposure. Objective : Reason why presently work had as objective to determine the spontaneous and induced frequency of transplacental micronucleis in Balb/c mice. Seeking to link this way the genotoxic and reproductive effect of a drug to evaluate for this methodology. Materials and Method : They were formed 4 experimental groups, the first a negative control (mockery), the second solvent control NaCl (0,9 %), in the third was used the cyclophosphamide in dose of 50 mg/kg, and the fourth was used the bleomycin in dose of 20 mg/kg. All the groups were administered for intraperitoneal route the 14, 15 and 16 days of the gestation and 24 h after the last inoculation was preceded to the sacrifice of the pregnant for cervical dislocation. Then they were obtained the maternal bone marrow and fetal liver samples. Results : We obtained the spontaneous and induced values of the citotoxicity and genotoxicity indexes as a result, as well as the micronucleus total divided according to levels of damages. Discussion or Conclusion : One observes bigger induction of damage in fetal hepatic cells that in maternal bone marrow cells. It was also demonstrated that the cyclophosphamide is able to induce bigger citotoxicity and genotoxicity that the bleomycin of the maternal bone marrow cells as in fetal hepatic cells. Therefore the transplacental clastogenic power of both mutagens was demonstrated linking this genotoxicity assays to the reproduction. These results could also be used in the evaluation of new drugs with antigenotoxic effects for transplacental route.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    0
    References
    0
    Citations
    NaN
    KQI
    []