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. Author manuscript; available in PMC: 2014 Jul 21.
Published in final edited form as: Ocul Surf. 2009 Oct;7(4):176–185. doi: 10.1016/s1542-0124(12)70185-4

Table 2.

Antioxidant-deficient rodent models displaying eye phenotypes

Gene Antioxidant deficiency Eye Phenotypes
Superoxide dismutase 1 (Sod1) Cytosolic CuZn-SOD Homozygous mutants are sensitive to diabetes-induced cataracts formation.37
Superoxide dismutase 2 (Sod2) Mitochondrial Mn-SOD Homozygous mutants show retinal pathologies before they die by 2.5 weeks.35
Superoxide dismutase 3 (Sod3) Extracellular CuZn-SOD Homozygous mutants show age-related loss of corneal endothelial cells and increased susceptibility to LPS-induced inflammatory endothelial damage.34
Glutathione peroxidase 1 (Gpx1) Cellular GPX Homozygous mutants show progressive lens pathologies with age and develop mature cataracts after 15 months.42
Aldehyde dehydrogenase 3A1 (Aldh3a1) ALDH3A1 Homozygous mutants develop cataracts and punctate opacities in lens cortex by 1 month.56
Aldehyde dehydrogenase 1A1 (Aldh1a1) ALDH1A1 Homozygous mutants develop cataracts at 6–9 months of age.56
Aldh3a1 and Aldh1a1 ALDH3A1 and ALDH1A1 Homozygous double mutants develop cataracts and punctate opacities in lens cortex by 1 month.56
γ-glutamyl transpeptidase1 (Ggt1) GSH Homozygous mutants develop bilateral cataracts by 2–3 months of age.81