The Role of Free Radicals Damage to the Optic Nerve and Vitreous After Ischemia

Abstract

Glaucoma is one of the major causes of blindness worldwide, affecting the retina and the optic nerve through injury inflicted by the elevated intra-ocular pressure (IOP). It is postulated that the pathological changes are a result of repeated episodes of ischemia and reperfusion in the ocular tissues, caused by the fluctuating IOP (Kalvin et al., 1966; Winterkorn and Beckman, 1995). In previous investigations, by us as well as by others, it was shown that transient ischemia most probably causes tissue damage through a burst of free radicals and non-radical oxygen derived active species (ROS) (Chevion et al., 1993; Ophir et al., 1993, 1994) and the combined action of other mechanisms, including: loss of energy stores, subsequent impairment of membrane transport processes, an accumulation of intracellular calcium followed by deregulation of calcium homeosatsis, and the release of potentially toxic substances such as excitatory amino acids. ROS, and particularly the highly reactive hydroxyl radical, could cause cellular damage by attacking a number of cellular components, including peroxidation of polyunsaturated fatty acids in membranes, inactivation of enzymes, and fragmentation of DNA molecules.