Carcinomas of the conjunctival epithelium are uncommon, and primary tumors of the corneal epithelium are rare. Tumors of exposed skin, including the eyelid, are common, and their frequency relates to sunlight exposure. This difference in cancer incidence suggests that the cornea in particular is protected against, or repaired exceptionally well after, UV damage or that a most effective mechanism eliminates neoplasms there. The objective is to determine which of these mechanisms protects the transparent epithelial tissues of the eye from the carcinogenic action of light. Obvious candidates for this protective role are UV adsorbers in the tear film or repair mechanisms that are not expressed in other epithelia because they, unlike the cornea, can be protected by anuclear squames or melanin, or because the tissues are not exposed to light. Our experiments will compare the extent of DNA damage and the rates of repair after irradiating different epithelia from rats and rabbits with long and short wavelength UV. Damage will be assessed by measuring the pyrimidine dimers in the purified DNA and the number of single-strand breaks produced by endonucleolytic scission under conditions where photorepair and repair synthesis are inhibited. Repair will be measured as photoreactivation of dimers, and the elimination of single-strand breaks. Strand nicks in the DNA will be estimated by measuring the distribution of chain lengths by alkaline gel electrophoresis and by measuring the rate of unwinding in alkali. Denaturation will be assessed by S1 nuclease digestion. Ara C will be used in experiments where repair synthesis will be inhibitied. Because mechanisms of repair novel to the cornea will not necessarily be detected by differences in repair rates, we will also compare the effects of repair inhibitors on kinetics of the elimination of damage from the irradiated tissues.
