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Related Concept Videos

  • Chemical Sciences
  • Medicinal And Biomolecular Chemistry
  • Characterisation Of Biological Macromolecules
  • Bee Venom Disrupts Vascular Homeostasis: Apitoxin And Melittin Trigger Vascular Cell Toxicity And Aortic Dysfunction In Mice.
  • Chemical Sciences
  • Medicinal And Biomolecular Chemistry
  • Characterisation Of Biological Macromolecules
  • Bee Venom Disrupts Vascular Homeostasis: Apitoxin And Melittin Trigger Vascular Cell Toxicity And Aortic Dysfunction In Mice.
  • Related Experiment Video

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    Bee venom disrupts vascular homeostasis: apitoxin and melittin trigger vascular cell toxicity and aortic dysfunction in mice.

    Àngel Bistué-Rovira1, Montse Solé2,3,4, Mateu Anguera-Tejedor1

    • 1Department of Pharmacology, Therapeutics, and Toxicology, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès (Barcelona), Spain.

    Toxicological Sciences : an Official Journal of the Society of Toxicology
    |June 11, 2025

    View abstract on PubMed

    Summary
    This summary is machine-generated.

    Bee venom (apitoxin) and its main component melittin can harm vascular cells and impair aortic function. These effects are linked to nitric oxide (NO) pathways and oxidative stress, highlighting potential risks alongside therapeutic uses.

    Keywords:
    endothelial dysfunctionnatural toxinsnitric oxideoxidative stresssex differencesvascular toxicity

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    Area of Science:

    • Vascular Biology
    • Toxicology
    • Pharmacology

    Background:

    • Bee venom (apitoxin), primarily composed of melittin, possesses therapeutic potential but its vascular toxicity is not well understood.
    • Understanding apitoxin's effects on vascular homeostasis is crucial for evaluating its safety in therapeutic applications.

    Purpose of the Study:

    • To investigate the impact of apitoxin and melittin on vascular cell viability and mouse aortic function.
    • To elucidate the mechanisms underlying apitoxin's vascular toxicity, focusing on nitric oxide (NO) and oxidative stress.

    Main Methods:

    • Cytotoxicity assays (MTT) were performed on cultured endothelial and smooth muscle cells.
    • Mouse aortic function was assessed by measuring isometric tension in response to various stimuli.
    • The roles of nitric oxide synthase (L-NAME) and antioxidant (SOD) were evaluated.

    Main Results:

    • Both apitoxin and melittin demonstrated dose-dependent cytotoxicity against vascular cells.
    • Apitoxin impaired phenylephrine-induced contractions and both endothelium-dependent/independent relaxations in mouse aortas, particularly in males.
    • Melittin mimicked these effects but at higher concentrations; NO pathway and oxidative stress were implicated in apitoxin's vascular toxicity.

    Conclusions:

    • Apitoxin and melittin reduce vascular cell viability and compromise aortic function at clinically relevant concentrations.
    • The findings highlight significant vascular risks associated with apitoxin, mediated by NO and oxidative stress.
    • This study underscores the need to balance the therapeutic potential of bee venom with its inherent vascular toxicity.