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Teratogen-induced apoptosis may be affected by immunopotentiation
V Toder1, S Savion, M Gorivodsky
1Department of Embryology and Teratology, Sackler School of Medicine, Tel-Aviv University, Israel.
Journal of Reproductive Immunology
|May 1, 1996
Summary
Intra-uterine immunization protects mouse embryos from cyclophosphamide (CP) toxicity by reducing CP-induced apoptosis. This immunopotentiation enhances embryo survival and fetal weight, suggesting a link between maternal immunity and teratogen response.
Area of Science:
- Immunology
- Developmental Biology
- Toxicology
Background:
- Cyclophosphamide (CP) is a known teratogen that induces embryotoxicity, partly through apoptosis.
- Intra-uterine immunization has previously shown potential in increasing embryo tolerance to CP-induced teratogenesis.
Purpose of the Study:
- To investigate if immunopotentiation can alter cyclophosphamide-induced apoptosis and protect against teratogenesis.
- To explore the role of fetomaternal immune interactions in the response to teratogens.
Main Methods:
- Mice underwent intra-uterine immunization with xenogeneic rat splenocytes before mating.
- Pregnant mice were treated with varying doses of cyclophosphamide (CP) on day 12 of gestation.
- Embryotoxic effects were assessed by implantation sites, resorptions, fetal malformations, and growth.
- Apoptosis was evaluated using flow cytometry and DNA fragmentation assays in embryonic tissues.
Main Results:
- High-dose CP caused significant embryonal death and growth retardation, with marked DNA fragmentation.
- Immunostimulation reduced embryonal loss by approximately 50% and increased fetal weight by about 30%.
- Reduced apoptosis levels in embryo cells correlated with improved fetal survival and weight in immunized mice.
- Low-dose CP-induced anomalies decreased in immunized females, alongside reduced apoptosis in fetal limbs and tails.
Conclusions:
- Intra-uterine immunization can mitigate cyclophosphamide-induced embryotoxicity.
- The protective effect of immunopotentiation appears to be mediated by a reduction in cyclophosphamide-induced apoptosis.
- Fetomaternal immune interactions may play a significant role in modulating teratogen-induced apoptosis.