The Role of Oxidative Stress in the Pathogenesis of Eye Diseases

Abstract

Oxidative stress can be defined as an excess of intracellular concentrations of reactive oxygen species (ROS). The term ROS is used to describe free radicals such as hydrogen peroxide, superoxide anion or singlet oxygen. All these chemical species are, as the term suggests, in a highly reactive state. Molecules with unpaired electrons in their outer orbits, such as free radicals, seek to react with other molecules to pair their unpaired electrons. ROS may occur as a natural by-product of the normal cellular metabolism of oxygen. Net cellular damage is a result of several factors, including the type and amount of free radicals, the rate at which they are produced, the structural integrity of the cell and its compartments, and the extent to which the antioxidative defense systems is active. Fortunately, the healthy human body has a number of ways to neutralize or eliminate ROS. Oxidative stress emerges when the ROS formation exceeds the capability of cells to clear and neutralize them. This is a harmful process that can negatively affect and damage macromolecules such as proteins and nucleic acids. Cells deploy an antioxidant defensive system to protect themselves from and repair ROS-induced cellular damage. If the body's repair mechanisms are also weakened, the resulting damage may lead to disease. In ophthalmology oxidative stress is a risk factor for the induction of several diseases such as glaucoma, Flammer-syndrome, age-related maculopathy or diabetic retinopathy.