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

Arsenic and urinary bladder cell proliferation.

Michael I Luster1, Petia P Simeonova

  • 1Inflammatory Disease Teams, Toxicology and Molecular Biology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505-2888, USA. mluster@cdc.gov

Toxicology and Applied Pharmacology
|July 28, 2004
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

Immune system evaluation of Echinacea Purpurea root extract in female Harlan Sprague Dawley (Hsd:Sprague Dawley SD) rats.

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association·2026
Same author

Assessment of immunotoxicity in the 21st century: Where we are and what we need to replace animals.

Current opinion in toxicology·2026
Same author

Investigation of the potential of bisphenol A substitutes to induce allergic contact sensitization using OECD defined approaches.

ALTEX·2026
Same author

Modification of the dextran sodium sulfate model to identify agents that induce or exacerbate inflammatory bowel disease.

Journal of immunotoxicology·2025
Same author

Immunotoxicity Studies on the Insecticide 2-((1-(4-Phenoxyphenoxy)propan-2-yl)oxy)pyridine (MPEP) in Hsd:Harlan Sprague Dawley SD<sup>®</sup> Rats.

Toxics·2025
Same author

Immunotoxicity assessment of multiwalled carbon nanotubes following whole-body inhalation exposure for 30 and 90 days in B6C3F1/N mice and 30 days in HSD:Harlan Sprague Dawley SD<sup>®</sup> rats.

Frontiers in toxicology·2025

Elevated arsenic in drinking water causes bladder uroepithelium hyperproliferation by activating specific signaling pathways. This arsenic accumulation in bladder tissue may promote carcinogenesis by increasing cell proliferation or mutation rates.

Area of Science:

  • Environmental toxicology
  • Cancer research
  • Molecular biology

Background:

  • Epidemiologic studies link elevated arsenic in drinking water to urinary bladder cancer.
  • The mechanisms underlying arsenic's carcinogenicity in the bladder are not fully understood.

Purpose of the Study:

  • To investigate the effects of sodium arsenite on the urinary bladder epithelium in vitro and in vivo.
  • To elucidate the molecular pathways involved in arsenic-induced bladder cell proliferation.

Main Methods:

  • Mice were exposed to 0.01% sodium arsenite in drinking water.
  • Analysis of arsenic accumulation in bladder tissue and urinary metabolites.
  • Assessment of MAP kinase pathway activation, including ERK, AP-1, and EGF receptor signaling.

Related Experiment Videos

Main Results:

  • Sodium arsenite exposure induced hyperproliferation of the bladder uroepithelium in mice.
  • Arsenic, primarily trivalent arsenite (iAs(3+)), accumulated in bladder tissue.
  • Arsenic activated the MAP kinase pathway, involving ERK, AP-1, and both EGF receptor-dependent and -independent events (Src activation).

Conclusions:

  • Arsenic accumulation in the urinary bladder epithelium triggers signaling pathways leading to chronic cell proliferation.
  • This arsenic-induced proliferation may contribute to bladder carcinogenesis through non-epigenetic mechanisms, such as increasing initiated cell proliferation or mutation rates.