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T. H. Wakamatsu, M. Dogru, Y. Sasaki, S. Ward, Y. Imamura, T. Shimizu, T. Shirasawa, J. Shimazaki, K. Tsubota; Tear Functions in the Superoxide Dismutase-1 Deficient (SOD-1-/-)Mice: An Animal Model for Dry Eye. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1919.
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The purpose of our study was to investigate the feasibility of the superoxide dismutase (SOD1)-deficient mice as a dry eye model.
Tear function tests (BUT and cotton thread), corneal sensitivity and corneal fluorescein staining tests were performed on SOD1- deficient mice (n=4) aged 18 ~ 23 weeks (average age= 20 weeks) and wild-type mice (n=5) aged 18 ~ 22 weeks (average age= 20 weeks). The mice were followed over 32 weeks, once a month. To collect the samples of tears from the mice we instilled a 10µl of PBS into the conjunctival sac and then tear fluid was collected with 10µl glass capillary tube by capillary action from the tear meniscus at the lateral canthus. Pro-inflammatory cytokines and chemokines in the tear fluid were analyzed by cytometric bead array test. The study was conducted in compliance with the ARVO statement for the use of animals in Ophthalmic and Visual Research.
Tear quantity values in SOD1-deficient mice were lower compared to the wild-type mice detected by the cotton thread test throughout the study . The mean corneal sensitivity and BUT values of the SOD mice were also consistently lower compared with wild type mice throughout the follow up. Fluorescein staining scores were higher in the SOD mice compared to the wild type mice throughout the study.Tear samples showed inflammatory changes.
The SOD-1 deficient mouse has been reported to be a model mouse of aging. Our preliminary results suggest that it may also serve as a mouse model of dry eyes, due to the abnormal quantitative and qualitative findings in the tears and ocular surface epithelium observed.
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