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K. Tsubota, Y. Sasaki, M. Dogru, Y. Imamura, T. Shirasawa, I. Saito; Oxidative Stress Decreases Tear Secretion in Cu,Zn–Superoxide Dismutase (SOD–1)–Deficient Mice . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5577.
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© ARVO (1962-2015); The Authors (2016-present)
The purpose of our study was to investigate the effect of oxidative stress in dry eye syndrome. We focused on the alteration of tear volume in Copper/zinc superoxide dismutase (SOD1)–deficient (–/–) mice.
SOD1–deficient (–/–) and C57BL6 strain wild–type (+/+) mice were used at 40 weeks of age. Collection of tears was performed after pilocarpine treatment (3mg/kg body weight). Tears were collected from three mice in each group for 15 min using calibrated microglass capillaries. All animals were weighed prior to each experiment. This study followed the guidelines on the Tenets and Declaration of Helsinki on Animal Research.
Pilocarpine–stimulated tear secretion in SOD1–deficient (–/–) mice (0.5±0.4 µL) was decreased (approximately one third) compared to the tear secretion in the wild–type (+/+) mice (1.5±0.3 µL)(P<0.05). Body weights were the same in SOD1–deficient (22.3±0.6g) and wild–type (21.3±0.6g) mice (P >0.05).
We demonstrated that oxidative stress might cause a decrease in tear secretion. Tear decrease was not dependent on the variations of body weight. Since SOD1 is one of the most important free radical scavenging enzymes in humans, further research based on our findings may pave the way to a new treatment approach in dry eye syndromes.
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