The effect of oxidative stress on intraocular pressure and retina in rats

• Main Authors: Chia-Ling Pai, 白佳靈
• Other Authors: Shiun-Long Lin
• Format: Others
• Language: zh-TW
• Published: 2014
• Online Access: http://ndltd.ncl.edu.tw/handle/63741419285001101190

碩士 === 國立中興大學 === 獸醫學系暨研究所 === 102 === An imbalance between oxidants and antioxidants in favor of the oxidants, potentially leading to damage, is termed ‘oxidative stress’. Oxidative stress causes damage to cells by protein oxidation, lipid peroxidation, glycol-oxidation, and DNA-oxidation. In the eye, it occurs large amounts of oxidative stress during transforming optical image to nerve impulses. For retina, the relationships between retinal degenerative disease including retinal pigmentosa (RP), ageing, age-related disease- age-related macular degeneration or elevation of intraocular pressure leading to retinal cell loss- glaucoma and oxidative stress are becoming the focus. Some studies indicate reactive oxygen species (ROS) may reduce the capability of antioxidants, increase in resistance of the aqueous humor drainage or induce the rearrangement of human trabecular meshwork and result in glaucoma finally. In this experiment, we try to verify the correlation between oxidative stress and intraocular pressure (IOP) and evaluate the effect of oxidative stress on retinal glial cells and inducible nitric oxide synthase. 8-week D-galactose injection was used to mimic high oxidative stress rats, and behavior tests, fundus images, anterior chamber depth, anterior chamber diameter and pupil diameter were investigated at the beginning and ending of induction. On the other side, IOP measurement per week and serum taking at pre-induction, fourth week, sixth week and eighth week for antioxidant capability of superoxide dismutase (SOD) and the amount of nitric oxide (NO). After perfusion, Müller’s cells and astrocytes, microglial and iNOS were labeled by GFAP, Iba-1 and iNOS immunofluorescence stainings. The locations and density of the glial cells and iNOS were analyzed. The activities of SOD and the concentration of NO in serum were decreased after induction. The spatial memory ability and muscular endurance were impaired through Morris water maze (MWM) and weight-loaded forced swimming test. These results demonstrated that oxidative stress was exacerbated by D-galactose. The IOP was gradually increased in 6th week after D-galactose induction, and no significant changes were found in fundus morphology. Angle-closure glaucoma was excluded by anterior segment-optical coherence tomography. Immunohistochemical stains showed that the density of Müller’s cells, astrocytes and microglia was increased after D-galactose induction. Microglia mostly became active. The location of iNOS was at inner nuclear layer (INL) and may appear at ganglion cell layer (GCL) and retinal pigment epithelium (RPE). These data indicate that oxidative stress may result in the impairment of behavior, elevation of IOP, increase of Müller’s cells, astrocyte and microglia which is induced by D-galactose. These may involve in the pathologies of aging or other neurodegenerative diseases. As for the elevation of IOP, more experiments are needed to unveil the detail of the mechanism.