AIM: To observe whether exposure to natural light causes damage on corneal tissue in infant rhesus monkeys with monocular hyperopic defocus induced by PRK.

METHODS: Twelve infant rhesus monkeys(aged 2mo)were treated monocularly with PRK(-4.0D)and divided into two groups: AL group(n=6)and NL group(n=6). The monkeys in AL were reared under artificial lighting(indoor).The monkeys in NL were exposed to natural lighting(outdoor)for 4h per day(9:00-11:00 and 15:00-17:00), and to indoor lighting for the rest of the light phase. Corneal haziness after PRK was assessed biomicroscopically using the Fantes scale. At 50d post-PRK, tear fluids of both eyes from 8 monkeys in the two groups(4 animals each group)were collected and analyzed for 11 kinds of cytokines using protein microarray analysis. At 180d post-PRK. The corneas were obtained and evaluated by histopathological examination, immunohistochemistry with antibody to TGF-β1 and α-SMA, and TUNEL. The vitality of SOD and the level of MDA in corneas were detected with WST-1 and lipid peroxidation MDA assay kits, respectively.

RESULTS: The monkeys in AL group exhibited a lesser degree of haze than those in NL group at 40d following PRK(P=0.015). At 50d post-PRK, EGF and TGF-β1 levels in tears were different in PRK-treated eyes between the two groups(P=0.045, 0.038), and TGF-β1 were significantly different between both eyes in the same group(AL: P=0.003; NL: P=0.036). At 180d post-PRK, there were no differences in histological changes, the expression of TGF-β1 and α-SMA, and apoptosis cell staining of the corneal between the two groups. The vatility of SOD and the levels of MDA in corneal epithelium were not different between the two groups(P>0.05).

CONCLUSION: Exposure to natural light in our study could not induce light damage to the normal cornea of the infant rhesus monkeys, but it could aggravate the corneal tissue repair reaction transiently post-PRK.