Cataract development in γ-glutamyl transpeptidase-deficient mice

Patricia Chévez-Barrios, Amy L. Wiseman, Emilio Rojas, Ching Nan Ou, Michael W. Lieberman

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


The present study was undertaken to analyse the relationship of lens glutathione (GSH) and light to cataract development in mice deficient in γ-glutamyl transpeptidase (GGT). These mice have reduced levels of cysteine and GSH in the eye and develop cataracts. GGT-deficient mice raised under normal vivarium conditions, showed no cataractous changes at birth, but by 1 week they had developed nuclear opacities. By 3 weeks more severe cataracts develop, and lens GSH levels are approximately 6-7 % of wild type levels. By 6-11 weeks cataracts show nuclear and cortical involvement, liquefaction and calcification. Single cell DNA electrophoresis (comet assay) demonstrated mild DNA damage in the lens epithelium. GGT-deficient mice raised in the dark beginning the day after conception all developed cataracts, but these were less severe than those in GGT-deficient mice raised with normal vivarium lighting. Administration of N-acetyl cysteine (NAC) raises lens GSH and almost completely prevents cataract development. Our data indicate that cataract development in GGT-deficient mice is multifactorial and results from exogenous damage (exposure to light), reduced lens GSH levels, and nutritional effects secondary to low cysteine levels. (C) 2000 Academic Press.

Original languageEnglish (US)
Pages (from-to)575-582
Number of pages8
JournalExperimental Eye Research
Issue number6
StatePublished - 2000


  • γ-glutamyl transpeptidase
  • Cataract
  • Cataract models
  • Cataractogenesis
  • DNA-damage
  • Glutathione
  • Light damage
  • N-acetylcysteine
  • Transgenic mice

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems


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