Retinal photic injury in normal and scorbutic monkeys

Mild and severe retinal photic injuries were inflicted on 22 eyes of seven monkeys fed a vitamin C-deficient diet and four monkeys given a vitamin C-enriched diet. The retinal lesions were studied by fundus examination, fluorescein angiography, and light and electron microscopy. While the general cellular response to photic injury in the retina of scorbutic animals was not different qualitatively from that in the normal animals, scurvy appeared to cause more severe tissue damage, an exaggerated repair response, and more advanced retinal degeneration. In the four groups of eyes, representing mild and severe photic injury in normal and scorbutic animals, a continous spectrum of changes was produced. The least damage occurred from mild photic injury in the normal animals, and the most detrimental insult resulted from severe photic injury in the scorbutic animals. We propose that the basic mechanism by which ascorbate mitigates retinal photic injury depends on its redox properties. Ascorbate functions as a antioxidant in the retina. It scavenges superoxide radicals and hydroxyl radicals, quenches singlet oxygen, and reduces hydrogen peroxide, all of which are formed in retinal photic injury. This hypothesis provides an explanation for the high level of ascorbate in the retina. The pathogenetic mechanisms that correspond to the three distinct phases of pathologic changes observed in retinal photic injury are characterized. In phase 1, singel oxygen is generated in a photodynamic reaction that damages the photoreceptor elements and pigment epithelium. In phase 2, macrophages attracted from the systemic circulation invade the subretinal space, and a photo-oxidative reaction generates superoxide radicals, hydrogen peroxide, and hydroxyl radicals. These free radicals attack the photoreceptor cells and pigment epithelium to cause further retinal damage. In phase 3, macrophages remain in the subretinal space for as long as 8 months after injury, causing persistent disruption of the blood-retinal barrier. The photo-oxidatve reaction appears to linger, resulting in chronic retinal degeneration. It is hypothesized that in some forms of age-related macular degeneration, patients suffer from repeated mild photic insult throughout their lifetime. Aging has been associated with subclinical scurvy, which leads to even greater susceptibility to photic injury. Although ascorbate moderates many biochemical functions of the body and helps the retina ameliorate photo-oxidative injury, it should be regarded as a nutritional supplement to maintain health when comsumed in appropriate amounts and not as a therapeutic agent for the treatment of severe insults.