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Related Experiment Videos

The early limb deformity caused by acetazolamide.

L B Holmes, R L Trelstad

    Teratology
    |October 1, 1979
    PubMed
    Summary

    Acetazolamide exposure during early gestation causes postaxial forelimb deformities in mouse embryos. This developmental issue arises from mesenchyme tissue deficiency, not cell death or impaired cartilage precursor aggregation.

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    Area of Science:

    • Developmental biology
    • Teratology
    • Pharmacology

    Background:

    • Acetazolamide is a carbonic anhydrase inhibitor used medically.
    • Drug-induced developmental abnormalities are a significant concern in prenatal health.
    • Understanding the mechanisms of teratogenesis is crucial for drug safety.

    Purpose of the Study:

    • To investigate the effects of acetazolamide on embryonic limb development.
    • To identify the timing and nature of acetazolamide-induced limb malformations.
    • To elucidate the cellular mechanisms underlying these deformities.

    Main Methods:

    • Histological examination of mouse embryonic forelimbs.
    • Timed pregnancies in C57Bl/6J mice exposed to acetazolamide.
    • Analysis of limb development at various embryonic stages post-exposure.

    Main Results:

    • Postaxial forelimb mesenchyme deficiency was observed in embryos.
    • Deformities were evident by embryonic day 10.9, 36 hours after a second acetazolamide dose.
    • The observed defect occurred prior to mesenchyme cell aggregation and chondrogenesis.
    • Cellular organization in adjacent mesenchyme was normal, suggesting acetazolamide's effect is not on initial precartilage aggregate formation.

    Conclusions:

    • Acetazolamide induces postaxial limb developmental defects in mice.
    • The primary mechanism involves mesenchyme tissue deficiency, not cell necrosis.
    • The drug's teratogenic effect appears to target early limb development processes beyond initial mesenchymal condensation.

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