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

Selenium salts and chromosome damage

S Biswas1, G Talukder, A Sharma

  • 1Department of Pathology, Vivekananda Institute of Medical Sciences, Calcutta, India.

Mutation Research
|May 23, 1997
PubMed
Summary
This summary is machine-generated.

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

CD28 ligation prevents bacterial toxin-induced septic shock in mice by inducing IL-10 expression.

Journal of immunology (Baltimore, Md. : 1950)·1997
Same author

MR imaging of tubercular spinal arachnoiditis.

AJR. American journal of roentgenology·1997
Same author

Interactions between transvenous nonthoracotomy cardioverter defibrillator systems and permanent transvenous endocardial pacemakers.

Pacing and clinical electrophysiology : PACE·1997
Same author

Role of the carboxyl-terminal region of Porphyromonas gingivalis fimbrillin in binding to salivary proteins.

Infection and immunity·1997
Same author

Phenethyl isothiocyanate modulates clastogenicity of mitomycin C and cyclophosphamide in vivo.

Mutation research·1996
Same author

Expression of functional Porphyromonas gingivalis fimbrillin polypeptide domains on the surface of Streptococcus gordonii.

Applied and environmental microbiology·1996
Same journal

Monoallelic germline RAD51C, RAD51D, and BRIP1 variants in hereditary cancer testing: Variant spectrum and clinical counselling implications.

Mutation research·2026
Same journal

Prediction of hepatocellular carcinoma associated biomarkers in TP53 gene; A comprehensive in silico analysis.

Mutation research·2026
Same journal

IDH1 mutation promotes angiogenesis via upregulation of hypoxia inducible factor 1 alpha in glial tumors.

Mutation research·2026
Same journal

Targeting overexpressed oncogenes in esophageal cancer through miRNA-mediated gene silencing: Insights from binding affinity and thermodynamic profiling.

Mutation research·2026
Same journal

The active compound quercetin from Polygonum cuspidatum targets COL3A1 to enhance CD8⁺ T cell cytotoxicity in gastric cancer.

Mutation research·2026
Same journal

E2F1 promotes LIHC malignant phenotype via NEK2-mediated Wnt/β-catenin and Notch activation and EMT.

Mutation research·2026
See all related articles

Sodium selenite and sodium selenate exposure caused chromosome breaks and spindle damage in mouse bone marrow cells. Higher chemical concentrations led to more severe genotoxic effects, with sodium selenite being slightly more potent.

Area of Science:

  • Environmental toxicology
  • Genetics and heredity
  • Cell biology

Background:

  • Selenium compounds are essential micronutrients but can be toxic at higher doses.
  • Understanding the genotoxic potential of different selenium forms is crucial for risk assessment.
  • Previous studies have indicated potential adverse effects of selenium on cellular processes.

Purpose of the Study:

  • To investigate the clastogenic and aneugenic effects of sodium selenite and sodium selenate.
  • To determine the dose-response relationship of these selenium compounds on bone marrow cells.
  • To compare the genotoxicity of sodium selenite versus sodium selenate.

Main Methods:

  • Age-matched male Swiss albino mice were gavaged with sodium selenite and sodium selenate.

Related Experiment Videos

  • Bone marrow cells were collected 24 hours post-administration.
  • Cells were processed using a colchicine-fixative-air drying-Giemsa staining schedule.
  • Chromosomal aberrations and spindle disturbances were analyzed.

    • Main Results:

    • Both sodium selenite and sodium selenate induced significant chromosomal breaks and spindle disturbances in mouse bone marrow cells.
    • The observed genotoxic effects were directly proportionate to the administered chemical concentrations (fractions of LD50).
    • Sodium selenite induced a slightly higher frequency of chromosomal aberrations compared to sodium selenate.

    Conclusions:

    • Sodium selenite and sodium selenate exhibit dose-dependent genotoxicity in mammalian bone marrow cells.
    • These selenium compounds can disrupt chromosomal integrity and mitotic spindle function.
    • Sodium selenite may possess a slightly greater clastogenic potential than sodium selenate at equivalent exposure levels.