FEB 22, 2011
Recent studies have shown that oxidative stress constitutes a major mechanism involved in the pathobiology of pseudoexfoliation (PEX) syndrome. Specifically, researchers have demonstrated that an increase in oxidative stress markers such as malondialdehyde and 8-isoprostaglandin-F2α, and a concomitant decrease in antioxidative protective factors such as ascorbic acid, catalase, and glutathione peroxidase, suggesting a faulty antioxidative defense system and increased oxidative stress in PEX.
Selenium is essential for the biologic functions of selenoproteins. Through these selenoproteins, selenium functions in the defensive mechanism for oxidative stress, in the regulation of thyroid hormone activity, and in the regulation of the redox status of vitamin C and other molecules. In several of its roles selenium functions as a dietary antioxidant and thus has been studied for its possible role in chronic diseases and glaucoma.
To investigate the possible role of selenium in the pathogenesis of PEX, the authors collected during cataract surgery aqueous humor, conjunctival specimens, and serum from 27 patients with pseudoexfoliation (PEX) syndrome and 20 age-matched patients without PEX syndrome.
Patients with PEX had significantly lower mean levels of selenium in aqueous humor and conjunctival specimens than controls (50.96 μg/L versus 77.85 μg/L and 4.04 μg/mg versus 7.19 μg/mg, respectively; P < 0.001). Mean selenium levels in serum of patients with PEX were also lower than in the control group (115.25 μg/L versus 124.25 μg/L), but this was not statistically significant.
The authors conclude that impaired antioxidant defenses in the eye may be associated with the pathogenesis of PEX syndrome. They advocate further studies on the role of essential trace elements in the development and pathogenesis of PEX.