Cataract Development in γ-Glutamyl Transpeptidase-deficient Mice

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 v...

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Bibliographic Details
Published in:Experimental eye research 2000-12, Vol.71 (6), p.575-582
Main Authors: Chévez-Barrios, Patricia, Wiseman, Amy L, Rojas, Emilio, Ou, Ching-Nan, Lieberman, Michael W
Format: Article
Language:English
Subjects:
Acetylcysteine - therapeutic use
Animals
Biological and medical sciences
cataract
Cataract - drug therapy
Cataract - enzymology
Cataract - etiology
cataract models
cataractogenesis
Cysteine - physiology
DNA-damage
Electrophoresis
Free Radical Scavengers - therapeutic use
gamma-Glutamyltransferase - deficiency
glutathione
Glutathione - physiology
Lens diseases
light damage
Lighting
Medical sciences
Mice
Mice, Inbred C57BL
N -acetylcysteine
Ophthalmology
transgenic mice
γ-glutamyl transpeptidase
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Summary: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.
ISSN:0014-4835
1096-0007
DOI:10.1006/exer.2000.0913