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

Adrenocortical involution in rats during oestrus synchronisation with medroxyprogesterone.

B F Fell, R M Campbell, D Dinsdale

    Research in Veterinary Science
    |May 1, 1977
    PubMed
    Summary

    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

    Correction: p73 and caspase-cleaved p73 fragments localize to mitochondria and augment TRAIL-induced apoptosis.

    Oncogene·2025
    Same author

    Metabolic reprogramming during neuronal differentiation.

    Cell death and differentiation·2016
    Same author

    Molecular profiling reveals primary mesothelioma cell lines recapitulate human disease.

    Cell death and differentiation·2016
    Same author

    Impact of carpal tunnel education on changing dental hygienists knowledge, risk behaviors, symptoms and functional performance.

    Work (Reading, Mass.)·2014
    Same author

    Thoracic outlet syndrome in musicians - an approach to treatment.

    Work (Reading, Mass.)·2014
    Same author

    Drosophila ref(2)P is required for the parkin-mediated suppression of mitochondrial dysfunction in pink1 mutants.

    Cell death & disease·2013

    Daily medroxyprogesterone acetate treatment caused adrenal atrophy in female rats by suppressing pituitary ACTH secretion. This study highlights apoptosis as a key mechanism in organ remodeling, with no significant liver changes observed.

    Area of Science:

    • Endocrinology
    • Cell Biology
    • Toxicology

    Background:

    • Medroxyprogesterone acetate is used for estrus synchronization.
    • Adrenocortical atrophy is a potential side effect of hormonal treatments.

    Purpose of the Study:

    • To investigate the effects of medroxyprogesterone acetate on the adrenal cortex.
    • To elucidate the cellular mechanisms underlying adrenocortical atrophy.

    Main Methods:

    • Female rats were administered daily medroxyprogesterone acetate injections.
    • Adrenocortical tissues were examined for cellular changes and apoptosis.
    • Biochemical and histological analyses of the liver were performed.

    Main Results:

    • Medroxyprogesterone acetate induced significant adrenocortical atrophy.
    Keywords:
    Adrenal Cortex EffectsAnimals, LaboratoryBiologyBody WeightClinical ResearchContraceptionContraceptive Agents, Female--administraction and dosageContraceptive Agents, Female--pharmacodynamicsContraceptive Agents, Progestin--administraction and dosageContraceptive Agents, Progestin--pharmacodynamicsContraceptive Agents--administraction and dosageContraceptive Agents--pharmacodynamicsCytologic EffectsEndocrine EffectsEndocrine SystemFamily PlanningHepatic EffectsHistologyLaboratory ProceduresLiterature ReviewMedroxyprogesterone Acetate--administraction and dosageMedroxyprogesterone Acetate--pharmacodynamicsPhysiologyResearch Methodology

    Related Experiment Videos

  • Extensive apoptosis (single cell deletion) was observed in the adrenal cortex.
  • No significant biochemical or histological changes were noted in the liver.

    • Conclusions:

    • Medroxyprogesterone acetate-induced adrenocortical atrophy is mediated by suppressed pituitary ACTH secretion.
    • Apoptosis plays a crucial role in organ remodeling processes.
    • The liver is not significantly affected by this treatment regimen.