The Role Oxidative Stress in the Pathogenesis of Eye Diseases: Currnt Status and a Dual Role of Physical Activity

Extensive research during the past three decades has demonstrated the mechanisms by which an imbalance in the redox status of prooxidant/antioxidant reactions in cells with advantage of prooxidant reactions (oxidative stress, OS) can cause peroxidation of nucleic acids, bases, lipids, proteins and carbohydrates, thus resulting in their damage. These actions result in stimulation of signal transduction pathways and activation of transcription factors that can lead to chronic inflammation and cause tissue dysfunction. The most important oxidants are reactive oxygen species (ROS) and reactive nitrogen species (RNS) generated by various metabolic pathways, physical, chemical and biological factors, and pathological conditions. The eye is one of the major target of the ROS/RNS attack due to exposition on several environmental factors like high pressure of oxygen, light exposure, ultraviolet rays, ionizing radiation, chemical pollutants, irritant, and pathogenic microbes, which are able to shift the redox status of a cell towards oxidizing conditions. There is increasing evidence indicating that persistent OS contributes to the development of many ocular diseases. Increases in the accumulation of hydrogen peroxide and markers of the oxidative damage to DNA, lipids, proteins observed in several eye diseases and usage of antioxidants in their treatment and prevention emphasize the involvement of OS pathways. This paper summarizes the present state of knowledge in the involvement of OS in the etiology of non-cancer ocular diseases (dry eye syndrome; corneal and conjunctive diseases; cataract; glaucoma; age-related macular degeneration; retinitis pigmentosa; diabetic retinopathy, autoimmune and inflammatory uveitis) and cancer ocular diseases (melanoma; retinoblastoma; lymphoma). The paper also discusses the potential applications of antioxidants in the prevention of eye diseases and shows a duality of physical exercise actions: protection against the ROS/RNS damage by regular-moderate physical activity and damaging effect through mediation of OS by endurance exercise without adaptable physical training.