Background. The role of metabolic changes in the anterior eye tissues in the pathogenesis of uveal inflammation in patients with elevated intraocular pressure has been studied poorly. Of particular interest, in this respect, are free radical mechanisms, which can be a trigger of oxidant stress and cause damage to cell membranes in ocular tissues. Purpose. To study the activity of pro-oxidant enzymes and levels of lipid peroxidation products in the uvea tissues in the rabbits with experimental anterior non-infectious uveitis against the background of ocular hypertension. Material and Methods. Forty-one rabbits were divided into 4 study groups. Group 1: 10 animals with experimental ocular hypertension; group 2: 10 animals with experimental allergic uveitis; group 3: 12 animals with ocular hypertension and allergic uveitis; and group 4: 9 intact animals serving as controls. To simulate ocular hypertension in the groups 1 and 3, the animals were made a single 0.1 ml injection of 0.3% carbomer into the anterior chamber. The tissues of the uvea and the aqueous humour were studied biochemically. We estimated the activity of pro-oxidant enzymes, NADPH oxidase and xanthine oxidase, and the content of lipid peroxides: malonic dialdehyde and diene conjugates. The data of the experimental studies were processed using parametric statistical tests with an SPSS package and Statistica 5.5 Results. The activity of pro-oxidants enzymes was increased in all uvea tissues in all study groups; the maximal NADPH oxidase and xanthine oxidase activity was in the animals with both ocular hypertension and uveitis. The NADPH oxidase and xanthine oxidase activity was increased by 51.1% and 63.9% (р<0.001), respectively, as compared with controls. Lipid peroxidation with accumulation of toxic products in the uvea and aqueous humour was noted both in the ocular hypertension-only and uveitis-only groups; however, the maximal values were in an uveitis model against the background of ocular hypertension, where malonic dialdehyde and diene conjugates were increased, respectively, by 67.0% and 54.3% (р<0.001) in the aqueous humour, and, respectively, by 93.1% and 69.1% (р<0.001) in the uvea tissues, compared with controls. Conclusions. Our findings reveal an important link in the pathogenic action of elevated IOP which burdens inflammation in the uveal tissues through the activation of oxidative and peroxidative processes. In addition, our findings support the assumption that primary high-pressure glaucoma can be a factor which worsens inflammation in the anterior eye.
Background: Senile cataract and glaucoma are the major age-related and degenerative ocular disorders that can cause loss of vision and blindness. To date, the question of the possible mechanisms involved in the impact of the glaucomatous process on the lens is still open. Purpose: To investigate the effect and mechanism of action of carnosine on the light-induced cataract model in the presence of experimental ocular hypertension (OHP). Materials and Methods: Rabbits were exposed to light from mercury arc-discharge lamps (type DRF-1000, 1000 W; bandpass range, 350-1150 nm) for 9 hours a day during a 10-week period to investigate the effect of regularly instilled (twice daily during the same period) carnosine on the development of opacities and thiol levels in the lens in the light-induced rabbit cataract model. OHP was induced bilaterally by injecting 0.1 mL of 0.3% carbomer solution into the anterior chamber of both eyes. Results: Mild changes in lens clarity (grades 1 to 3) were more common in rabbits treated with carnosine, whereas more apparent changes in lens clarity were more common in untreated animals. At 10 weeks, grade 5 lens opacity was noted in 8.3% of the rabbits treated with carnosine and in 20.3% of the untreated animals. Introduction of carnosine in the rabbit model of light-induced cataract in the presence of OHP resulted in 49.2% increase in the reduced glutathione levels, 28.3% decrease in oxidized glutathione levels, 40.7% increase in the sulfhydryl (thiol) levels and 28% decrease in the disulphide levels in the lenses of treated experimental animals compared to untreated experimental animals. Conclusion: A long-term intraocular treatment with carnosine in the rabbit cataract model (a) improved the resistance of the lens to cataractogenic phototoxicity in the presence of ocular hypertension and (b) contributed to substantial normalization of thiol levels in the lens, thus preventing oxidative damage to proteins.
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