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Enhanced age‐related and diabetes‐induced cataract in mice lacking CuZn‐superoxide dismutase
Author(s) -
OLOFSSON EM,
MARKLUND SL,
BEHNDIG A
Publication year - 2009
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2009.3444.x
Subject(s) - sod1 , reactive oxygen species , oxidative stress , superoxide dismutase , diabetes mellitus , antioxidant , medicine , endocrinology , type 2 diabetes , oxidative phosphorylation , glutathione , cataract surgery , chemistry , biochemistry , ophthalmology , enzyme
Purpose In the lens, light and oxygen generate harmful reactive oxygen species (ROS) that may cause age‐related cataract. In diabetes mellitus, increased glucose levels may contribute to increased generation of ROS which may accelerate cataract formation. We have here explored the role of the antioxidant enzyme copper‐zinc superoxide dismutase (SOD1) in the protection against age‐related and diabetes‐induced cataract development. Methods Cataract formation in relation to the oxidative status of the lens was evaluated in streptozotocin‐induced diabetic as well as in non‐diabetic SOD1 null and wild‐type mice. Also, the spontaneous age‐related cataract development was followed in both genotypes. Results Cataract was seen in the SOD1 null and the wild‐type mice after 8 weeks of diabetes, although the SOD1 null mice showed a more pronounced cataract formation than the wild‐type mice in relation to the level of hyperglycaemia. As cataract formation was accentuated the lenses showed diminishing levels of glutathione but increasing amounts of protein carbonyls, suggesting a reduced lens anti‐oxidative capacity as well as increased lens protein oxidation. Spontaneous incipient age‐related cataract was seen in the 1‐year old SOD1 null mice whereas the wild‐type mice showed equivalent changes at 2 years of age. Conclusion The results presented here show that SOD1 null mice are more prone to develop diabetes‐induced and age‐related cataract than wild‐type mice. The findings thus further endorse the importance of oxidative stress as a contributor to cataract development and indicate that superoxide radicals may be damaging to the lens. We therefore conclude that the antioxidant enzyme SOD1 is important for the protection against cataract.