Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Pharmacological concepts and developmental toxicology.

R G Skalko1

  • 1Department of Anatomy, East Tennessee State University, Quillen-Dishner College of Medicine, Johnson City 37614.

Annals of the New York Academy of Sciences
|January 1, 1989
PubMed
Summary

Developmental toxicants (teratogens) may disrupt embryonic development by altering time-dependent signal-response pathways. Validating this requires demonstrating dose-dependency, pharmacokinetic correlation, and specific toxicant receptors.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Developing allantois is a primary site of 2'-deoxycoformycin toxicity.

Teratology·1996
Same author

Reproductive and developmental toxicity of the components of gasoline.

Environmental health perspectives·1993
Same author

Occurrence of embryotoxicity in mouse embryos following in utero exposure to 2'-deoxycoformycin (pentostatin).

Teratology·1993
Same author

Adenosine levels in the postimplantation mouse uterus: quantitation by HPLC-fluorometric detection and spatiotemporal regulation by 5'-nucleotidase and adenosine deaminase.

Developmental dynamics : an official publication of the American Association of Anatomists·1992
Same author

Effects of (R)-deoxycoformycin (pentostatin) on intrauterine nucleoside catabolism and embryo viability in the pregnant mouse.

Teratology·1992
Same author

Axonal guidance of adenosine deaminase immunoreactive primary afferent fibers in developing mouse spinal cord.

Brain research bulletin·1990

Area of Science:

  • Developmental toxicology
  • Pharmacology
  • Embryology

Background:

  • Developmental toxicants, or teratogens, pose risks to embryonic development.
  • The precise mechanisms by which teratogens exert their effects are not fully understood.
  • Existing frameworks often lack a mechanistic basis rooted in pharmacological principles.

Purpose of the Study:

  • To propose and provide evidence for a novel hypothesis regarding teratogen action.
  • To frame the biological activity of developmental toxicants using established pharmacological principles.
  • To highlight the importance of signal-response mechanisms in teratogenesis.

Main Methods:

  • Review and synthesis of existing evidence on developmental toxicants.
  • Application of pharmacological concepts such as dose-response relationships.

Related Experiment Videos

  • Consideration of pharmacokinetic parameters and receptor binding in toxicological effects.
  • Hypothesizing the role of time-dependent signal-response pathways in the embryo.
  • Main Results:

    • Evidence is presented to support the concept that teratogens interfere with or enhance embryonic signal-response mechanisms.
    • The hypothesis necessitates demonstrating a functional relationship between administered dose and observed effect.
    • Positive correlation between toxicant effects and pharmacokinetic parameters is crucial.
    • The existence of specific receptors for toxicants is a key component of the proposed mechanism.

    Conclusions:

    • Developmental toxicants likely act by modulating critical time-dependent signal-response pathways within the developing embryo.
    • Further research is needed to fully validate this mechanistic framework.
    • Applying pharmacological principles offers a valuable approach to understanding teratogen activity and establishing a mechanistic basis for developmental toxicity.