| First Author | Chévez-Barrios P | Year | 2000 |
| Journal | Exp Eye Res | Volume | 71 |
| Issue | 6 | Pages | 575-82 |
| PubMed ID | 11095909 | Mgi Jnum | J:66279 |
| Mgi Id | MGI:1928223 | Doi | 10.1006/exer.2000.0913 |
| Citation | Chevez-Barrios P, et al. (2000) Cataract development in gamma-glutamyl transpeptidase-deficient mice. Exp Eye Res 71(6):575-82 |
| abstractText | The present study was undertaken to analyse the relationship of lens glutathione (GSH) and light to cataract development in mice deficient in gamma-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. Copyright 2000 Academic Press. |
