Oxygen free radicals and corneal endothelium

Abstract

We have demonstrated that corneal endothelial cells are susceptible to damage from hydrogen peroxide. Hydrogen peroxide perfusion of corneal endothelium results in physiologic and anatomic disruption of corneal endothelial cells with resulting swelling of the corneal stroma. Enzymatically generated superoxide anion produced endothelial damage which could not be blocked with superoxide dismutase (which removes superoxide anion from the system), but could it be blocked with catalase which removes hydrogen peroxide from the system. This indicated that the superoxide anion was not the toxic agent, but rather hydrogen peroxide, its dismutation product. Enzymatically generated oxygen free radical in the anterior chamber of the rabbit eye resulted in an increased iris vascular permeability which persisted for up to 24 hours following anterior chamber injection of hypoxanthine and xanthine oxidase. Young animals were better able to withstand oxidative stress to the eye then were older animals. The physiologic effects of oxidative stress in young animals can be made comparable to that in the older animals by depletion of catalase with 3-aminotriazole.