JAN 08, 2013
This experimental study found that a lack of copper-zinc superoxide dismutase, an intracellular anti-oxidant enzyme, may enhance the formation of age-related lens opacities in vivo in mice protected against known environmental risk factors for cataract development.
The authors investigated the development of lens opacities in copper-zinc superoxide dismutase-lacking mice and wild-type mice of various ages. The 18-week-old mice of both genotypes had clear lenses. However, mice lacking copper-zinc superoxide dismutase had developed cortical lens opacities by age one, whereas the wild-type mice did not show equivalent changes until two years of age. Lens carbonyls increased over time in both types of mice, while glutathione decreased only in the 2-year-old wild-type mice.
They note that studies involving the same wild-type mice have shown mild, progressive lens clouding mainly appearing late in life between 78 and 95 weeks of age, which concur well with the findings in this study. This delayed cataract development in the wild-type mice may be due to an age-dependent inactivation of the superoxide dismutase isoenzymes.
They also note that comparable levels of carbonylated proteins were found in both genotypes. Thus, oxidants causing the lens opacities in the copper-zinc superoxide dismutase-lacking mice may be in part different from those causing protein carbonylation. Cataract formation also may relate to levels of the anti-oxidant glutathione and its interaction with copper-zinc superoxide dismutase.