The current study’s goal was to promote ocular treatments by using a three-dimensional (3D) corneal epithelial tissue model to examine dry eye disease and oxidative stress-related corneal epithelial damage. Normal human corneal epithelial cells were grown in air-liquid interface cultures to create 3D corneal epithelial tissues suitable for physiologically relevant exposure to environmental variables. By subjecting the tissues to non-toxic amounts of ultraviolet (UV), hydrogen peroxide, the vesicant nitrogen mustard, or desiccating circumstances, oxidative stress was created. These stimuli induced morphological, cellular, and molecular alterations related to dry eye illness. Barrier function, tissue viability, reactive oxygen species (ROS) accumulation, lipid peroxidation, cytokine release, histology, and gene expression were all assessed as part of the evaluation of the specific responses in the cornea. Key elements of molecular responses to diverse types of oxidative stress-induced ocular injury were physically and functionally replicated in a 3D corneal epithelial tissue model. The effects of UV irradiation, hydrogen peroxide exposure, nitrogen mustard exposure, and desiccating circumstances on intracellular ROS buildup, barrier disruption, lipid peroxidation, and IL-8 release were the most notable ones for each treatment.
