UVA-induced oxidative damage in retinal pigment epithelial cells after H2O2 or sparfloxacin exposure

Retinal impairment is one of the leading causes of visual loss in an aging human population. To explore a possible cause for retinal damage in the hum an population, we have monitored DNA oxidation in human retinal pigment epi thelial (RPE) cells after exposure to hydrogen peroxide (H2O2) or the quino lone antibacterial sparfloxacin. When H2O2- or sparfloxacin-exposed cells w ere further exposed to ultraviolet A (UVA) irradiation, oxidative damage to the DNA of these cells was greatly increased over baseline values. This RP E+pharmaceutical-UVA cell system was developed to mimic in vivo retinal deg eneration, seen in mouse studies using quinolone and UVA exposure. DNA dama ge produced by sparfloxacin and UVA in RPE cells could be remedied by the u se of antioxidants, indicating a possible in vivo method for prevention or minimization of retinal damage in humans