Ultraviolet radiation-induced corneal degeneration in 129 mice

Kimberly M Newkirk1, Heather L Chandler, Allison E Parent

  • 1Department of Veterinary Biosciences, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio 43210, USA. kmnewkirk@mail.ag.utk.edu

Toxicologic Pathology
|October 19, 2007
PubMed

Insights

Ultraviolet radiation (UVR) causes significant ocular damage in mice, including keratocyte loss and cataracts. UVR-induced apoptosis is proposed as the mechanism behind these observed corneal and lens lesions.

Area of Science:

  • Ophthalmology
  • Photobiology
  • Toxicology

Background:

  • Ultraviolet radiation (UVR) is a known risk factor for human ocular diseases.
  • Previous studies have not extensively detailed UVR-induced ocular lesions in mice.

Purpose of the Study:

  • To investigate and characterize ocular lesions in mice chronically exposed to UVR.
  • To identify the cellular mechanisms responsible for UVR-induced ocular damage.

Main Methods:

  • Chronic UVR exposure in mice as part of a skin carcinogenicity study.
  • Histological examination of globes to identify ocular lesions.
  • Immunohistochemistry for cleaved caspase 3 to detect apoptosis.

Main Results:

  • Chronic UVR exposure led to significant ocular lesions in all affected globes.
  • A primary lesion of marked keratocyte loss was observed, not previously reported in UVR-exposed mice.
  • Secondary lesions included corneal thinning, keratoconus, vascularization, fibrosis, keratitis, globe rupture, and phthisis bulbi.
  • Spontaneous cataracts were prevalent in both UVR-exposed and unexposed mice, with a notable occurrence in 129 mice.
  • Acute UVR exposure induced apoptotic cells in the corneal epithelium and stroma.

Conclusions:

  • UVR causes a spectrum of severe ocular lesions in mice.
  • UVR-induced apoptosis is the likely mechanism for keratocyte loss in the cornea.
  • The high incidence of spontaneous cataracts in 129 mice warrants further investigation.

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