Light-induced formation of oxygen free radicals has been proposed as the underlying mechanism of photic retinal injury. We investigated the role of hydroxyl radical in retinal photic injury by treating dark-adapted albino rats with intraperitoneal dimethylthiourea 3 hours before exposure to intense fluorescent light. Dimethylthiourea is a specific antioxidant against hydroxyl radical. We demonstrated that dimethylthiourea penetrates well into retinal tissue and has a half-life of approximately 19 hours. Morephologic differences between the control and dimethylthiurea-treated rats were not remarkable 6 hours after light exposure, but they became significant 6 and 14 days after light exposure. Morphometric studies showed that there was significantly better preservation of photoreceptor nuclei in dimethylthiourea-treated rats 6 and 14 days after light exposure. Rhodopsin levels were significantly higher in the dimethylthiourea-treated rats 6 hours and 14 days after light exposure, while rhodopsin levels were comparable in the control and dimethylthiourea-treated rats 6 days after exposure. The differences in morphometry and rhodopsin levels between the control and dimethylthiourea-treated rats were statistically significant in relationship to dimethylthiourea treatment. The superior and temporal retinal quadrants appeared most vulnerable to photic injury in control rats 6 and 14 days after light exposure. These findings indicate that dimethylthiourea ameliorates retinal photic injury, and that hydroxyl radical plays an important role in mediating retinal photic injury.