Comparative antioxidant activity of various ophthalmic product types for artificial tears under different experimental conditions

Abstract

Artificial tears or lubricants is a developing category in pharmaceutical research, due to the permanent increasing incidence of dry eye syndrome caused by the extensive use of personal computers and other gadget screens, associated with global warming and pollution. Considering the role of inflammation in dry eye syndrome, characterized by the production of free radicals, it is imperative to determine which elements are more significant in forming an artificial tear more effectively and more comfortably for the eye state and for the quality of life. Thus, the aim of the present study was to examine the evolution of the total antioxidant capacity of some frequently commercialized artificial tears via the photochemiluminescence method, using an antioxidant capacity of lipid soluble substances procedure, prior and subsequent to the exposure of these therapy agents to some physical agents. This is a preliminary research aiming to evaluate the impact of various environmental factors on these ophthalmic products, to be continued by evaluating whether the effectiveness of these products, in terms of objective examination and patient preference and adherence criteria, is impacted by the conditions of use and storage. Thus, the total antioxidant capacity of the evaluated artificial tear samples after UVC irradiation at 254 nm wavelength was studied, in order to investigate whether their status suffered any change in terms of antioxidant potential. In addition to the findings obtained in the study, some recommendations were also made.

Chlorine-Induced Toxicity on Murine Cornea: Exploring the Potential Therapeutic Role of Antioxidants

“…These samples can be indirectly assessed for antioxidant effects through oxidative stress and superoxide staining [ 74 ]. Direct assessment can be achieved using the Trolox Equivalent Antioxidant Capacity method [ 52 , 76 , 77 ]. Furthermore, we hypothesize that Cl 2 -induced ROS triggers mitochondrial dysfunction.…”