Oxidative stress as a trigger for the infl ammatory process and dystrophic changes in the lens during cataractogenesis

Abstract

Introduction: At the heart of the pathogenesis of various diseases of the visual organ is the depletion of the system of antiradical protection of eye tissues. Our attention was drawn to the infl uence of the infl ammatory process in the cornea on the stability of the lens and on metabolic changes in the formation of cataracts. Aims: To determine the level of imbalance of the pro-antioxidant system in the eye tissues of rabbits and patients with cataracts with concomitant infl ammatory process in the cornea. Methods: Preclinical studies have been performed in chinchilla rabbits with light cataracts. Glutathione peroxidase, catalase, and lipid peroxidation products, malonic dialdehyde ( MDA) and diene conjugates ( DC), were determined in lens, chamber moisture, and tear fl uid. Clinical studies have been performed in patients with stromal bacterial keratitis and in somatically healthy individuals. In the tear fl uid of patients was determined by the total antioxidant activity ( TAA), the content of MDA and DC. Results: It was found that the level of glutathione peroxidase activity in the lens of rabbits with keratitis is reduced by 25.0% (p < 0.05), and catalase by 22.1% (p < 0.05), with light cataract–by 30.0 and 26.0%, with light cataract on the background of keratitis–by 33.8 and 28.7%, compared with the norm, respectively. The development of keratitis led to an increase in the lens of rabbits MDA level–by 23.2% (p < 0.05), DC–by 17.4% (p > 0.05), with light cataract–by 31.7% (p <0.01) and 26.1% (p < 0.05), with light cataracts on the background of keratitis–by 41.5% (p < 0.001) and 34.8% (p < 0.01) compared with the norm. There was a strong negative correlation between the indicators of MDA and TAA tear fl uid of patients: in patients with keratitis r = –0.78 (p < 0.01), in patients with keratitis with lens opacity r = –0.89 (p < 0.01). Conclusions: Concomitant infl ammatory processes in the cornea have a pathogenic eff ect on the lens and exacerbate degenerative changes in the lens in the experiment and in sick patients. This is due to their destabilizing eff ect on the prooxidant-antioxidant balance in the tissues of the eye that are in a state of oxidative stress. Accumulation of peroxidation products in the tissues of the eye of experimental animals and patients with cataracts on the background of depletion of the antioxidant system are a trigger in the infl ammatory process of dystrophic changes in the lens.