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Related Experiment Videos

Embryonic development and mitochondrial function. 2. Thiamphenicol induced embryotoxicity.

R Bass, D Oerter

    Naunyn-Schmiedeberg'S Archives of Pharmacology
    |February 1, 1977
    PubMed
    Summary
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    Inhibiting mitochondrial protein synthesis, like with thiamphenicol (TAP), impairs embryonic development by affecting DNA synthesis. Sensitivity and dosage requirements change with embryonic age and placental development.

    Area of Science:

    • Developmental Biology
    • Toxicology
    • Biochemistry

    Background:

    • Mitochondrial protein synthesis is crucial for embryonic development.
    • Inhibition of mitochondrial function can lead to developmental abnormalities.

    Purpose of the Study:

    • To investigate the effects of inhibiting mitochondrial protein synthesis on rat embryonic development.
    • To determine the impact of thiamphenicol (TAP) on embryonic DNA synthesis and growth.

    Main Methods:

    • Administered thiamphenicol (TAP) to pregnant rats at different gestational stages.
    • Measured cytochrome oxidase (cytox) activity as an indicator of mitochondrial protein synthesis.
    • Assessed DNA synthesis and embryonic growth parameters.

    Main Results:

    Related Experiment Videos

    • TAP inhibited mitochondrial protein synthesis (cytox activity) and subsequently impaired DNA synthesis and embryonic growth.
    • Embryos on days 10-11 were more sensitive to TAP than on day 9.
    • Placentation (day 12) altered TAP dosage requirements.
    • Dose-response varied with treatment duration; prolonged treatment (4 days) required lower doses.
    • Higher doses led to embryolethality.

    Conclusions:

    • Mitochondrial protein synthesis inhibition during late organogenesis significantly impairs rat embryonic development.
    • Embryonic sensitivity to TAP-induced developmental toxicity is stage-dependent.
    • Factors like growth rate, mitochondrial content, ATP availability, and placental transfer influence developmental outcomes.