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Age-related cataract progression in five mouse models for anti-oxidant protection or hormonal influence.

Authors: Wolf, N  Penn, P  Pendergrass, W  Van Remmen, H  Bartke, A  Rabinovitch, P  Martin, GM 
Citation: Wolf N, etal., Exp Eye Res. 2005 Sep;81(3):276-85.
Pubmed: (View Article at PubMed) PMID:16129095
DOI: Full-text: DOI:10.1016/j.exer.2005.01.024

Five mouse models with known alterations of resistance to oxidative damage were compared by slit lamp examination for the presence and degree of advancement of age-related cataract in young adult and old animals along with wild type controls. A group of young and old normal C57BL/6Jax mice were examined first to constitute a standard, and they were found to exhibit age-related cataract development. Following this, four models on the C57BL/6 background with imposed genetic alterations affecting anti-oxidant enzyme presence or activity, and one outbred model in which a deletion blocked the growth hormone/IGF-1 axis, were similarly examined. There was no evidence of foetal or juvenile cataract development in any of these models, and an age-related severity for lens opacities was shown between young adult and old mice in all groups. Model 1, mice null for the anti-oxidant gene glutathione peroxidase-1 (GPX1) had significantly advanced cataracts in older mice vs. same age controls. In mouse model 2 hemizygous knockout of SOD2 (MnSOD) did not affect age-related cataract development. In model 3 combining the GPX1 and SOD2 deficiencies in the same animal did not advance cataract development beyond that of the GPX1 null alone. In model 4 the addition of anti-oxidant protection in the lens by transfection of human catalase targeted only to the mitochondria resulted in a significant delay in cataract development. The 5th model, growth hormone receptor knockout (GHR-/-) mice, also demonstrated a significant reduction in age-related cataract development, as well as dwarfism. These findings, in general, support the oxidative theory of age-related cataract development. The exception, the partial deletion of SOD2 in the hemizygous KO model, probably did not represent a sufficiently severe deprivation of anti-oxidant protection to produce pathologic changes in the lens.

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RGD ID: 10003112
Created: 2015-05-01
Species: All species
Last Modified: 2015-05-01
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.