Experimental cataract induced by ultraviolet radiation.

The purpose of the present work was to increase the understanding of the toxic effects of ultraviolet radiation on the lens. A high-pressure mercury arc source with collimating optics, an interference filter (Tmax = 300 nm, T0.5 = 10 nm) and projecting optics was employed for experimental exposure of animals. Irradiance was measured with a calibrated photodiode. A device for objective absolute measurement of light dissemination in rat lenses was developed and characterized on a reference sample of lenses from healthy rats. A tolerance limit for non-pathological was set on a statistical basis. A method for preparing lens samples for atomic absorption spectrophotometry was developed and characterized. In vivo exposure of rat lenses to 6 kJ/m2 induced unscheduled DNA synthesis and reduced scheduled DNA synthesis. Microscopic observation, with a phase contrast microscope, of rat lenses demonstrated that in vitro exposure to 0.72 and 2.9 kJ/m2 evoked anatomical alterations in the lens epithelial cells and accelerated the swelling observed in incubated lenses. Lenses exposed to 36 kJ/m2 in vivo opacified completely in one week. The exclusively white opacification started at the anterior surface. As observed light and electron microscopically the lens cells swelled, starting in the epithelium and thereafter involving first the anterior cortex, later the posterior cortex and finally, within a week after exposure, the outer nuclear region. Light dissemination in the lens after exposure to 30 kJ/m2 increased exponentially with a 5.5 h latency before onset, and a time constant of 19 h. The water mass in the same lenses increased transiently with a maximum 24 h after exposure. The expected increase in lens dry mass due to growth did not take place. Rabbit lenses were incubated after exposure in vitro to 0.6, 3.0 and 6.0 kJ/m2, respectively. The two higher doses induced quicker mass gain in exposed lenses than in their non-exposed contralaterals. There is an increase in sodium in lenses exposed to 30 kJ/m2 and a simultaneous decrease in potassium. The sodium increased exponentially with a 6.6 h latency before onset, and a time constant of 38 h. A slight increase in light dissemination and in sodium per dry mass was noted even in the non-exposed lenses contralateral to those exposed. The data collected suggest that the opacification seen after a high-dose exposure of the lens to 300 nm UVR in vivo occurs as a result of osmotic swelling.