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Enhanced age‐related cataract in copper‐zinc superoxide dismutase null mice
Author(s) -
Olofsson Eva M,
Marklund Stefan L,
Behndig Anders
Publication year - 2012
Publication title -
clinical and experimental ophthalmology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.3
H-Index - 74
eISSN - 1442-9071
pISSN - 1442-6404
DOI - 10.1111/j.1442-9071.2012.02794.x
Subject(s) - superoxide dismutase , reactive oxygen species , zinc , dismutase , oxidative stress , sod1 , antioxidant , lens (geology) , medicine , biochemistry , endocrinology , chemistry , biology , paleontology , organic chemistry
A bstract Background: As the lens is constantly exposed to light and oxygen that generate harmful reactive oxygen species, the importance of the intracellular antioxidant enzyme copper‐zinc superoxide dismutase for the protection against age‐related cataract development was explored. Methods: The development of lens opacities and the lens oxidative status were studied in different age groups of mice lacking copper‐zinc superoxide dismutase and in wild‐type mice. The lens opacities were quantified from lens photographs using digital image analysis. Thereafter, the lenses were homogenized and analysed regarding their contents of reduced glutathione and protein carbonyls suggestive of protein oxidation. Results: The 18‐week‐old mice of both genotypes had clear lenses. At 1 year of age, the copper‐zinc superoxide dismutase null mice had developed cortical lens opacities, whereas the wild‐type mice did not show equivalent changes until 2 years of age. The lens contents of glutathione decreased only in the 2‐year‐old wild‐type mice, whereas the carbonyls increased over time without any differences between the two genotypes. Conclusions: This study indicates that the lack of copper‐zinc superoxide dismutase may accelerate age‐related lens opacity development and that intracellular superoxide‐derived oxidative stress may be damaging to the lens during ageing. Participation of the anti‐oxidant enzyme copper‐zinc superoxide dismutase in the protection against age‐related cataract was thus suggested.