Under physiologic conditions, reactive oxygen species (ROS) participate in normal biochemical processes, where they either act as intermediaries or function as second messengers. Also, ROS can be generated by exogenous influences, such as exposure to ultraviolet (UV) light or cigarette smoking. Oxidative stress occurs when the production of ROS exceeds their degradation.
Unchecked, ROS injure cell membranes and DNA, leading to tissue damage and cell death. ROS, like free radicals, react with unsaturated fatty acids that are present within cells and cell membranes, forming lipid peroxides. The oxidation of membrane phospholipids has been hypothesized to increase the permeability of cell membranes and/or inhibit membrane ion pumps. This loss of barrier function is thought to lead to edema, disturbances in electrolyte balance, and elevation of intracellular calcium levels, all of which contribute to cell malfunction and, potentially, to cell death. Free radical–mediated DNA damage can also lead to cell death through induction of apoptosis.
The resultant loss of cells leads to dysfunction in the eye, whether at the level of the trabecular meshwork and retinal ganglion cells (RGCs) in glaucoma, the inner retina in diabetic retinopathy, or the outer retina in age-related macular degeneration (AMD).
Excerpted from BCSC 2020-2021 series: Section 2 - Fundamentals and Principles of Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.