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Perinatal hepatocarcinogenesis.

S D Vesselinovitch

    Biological Research in Pregnancy and Perinatology
    |January 1, 1983
    PubMed
    Summary

    Perinatal exposure to chemical carcinogens is more potent in mice than adult exposure. Infant mice showed higher susceptibility than fetuses due to enzymatic activation and rapid cell replication, suggesting a link to late development.

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    Certain aspects of hepatocarcinogenesis in the infant mouse model.

    Toxicologic pathology·1987

    Area of Science:

    • Toxicology
    • Developmental Biology
    • Carcinogenesis

    Background:

    • Mouse development extends postnatally, making late-stage intrauterine development occur after birth.
    • This unique developmental timeline influences the impact of environmental exposures on carcinogenesis.

    Purpose of the Study:

    • To investigate the differential hepatocarcinogenic effects of specific chemical agents (benzidine, safrole, amitrol, ENU, DEN) based on exposure timing (perinatal vs. adult).
    • To compare the susceptibility of fetal versus infant mice to chemical carcinogens during the extended perinatal development phase.

    Main Methods:

    • Exposure of B6C3F1 mice to benzidine x 2HCl, safrole, amitrol, ethylnitrosourea (ENU), and diethylnitrosamine (DEN) at different life stages: transplacentally, postnatally, and during adulthood.
    • Assessment of chemically induced hepatocarcinogenesis across the different exposure groups.

    Main Results:

    • Perinatal exposure to the studied agents demonstrated significantly higher hepatocarcinogenicity compared to adult exposure.
    • Infant mice exhibited greater responsiveness to the carcinogens than fetal mice.
    • Higher susceptibility in infants is linked to the enzymatic machinery for procarcinogen activation and high macromolecular replication rates.

    Conclusions:

    • Carcinogenesis in infant mice can be considered an extension of late intrauterine development.
    • Findings suggest potential risks for other species exposed to these carcinogens during their analogous late developmental phases.

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