The purpose of this study was to investigate if topically applied caffeine protects against in vivo ultraviolet radiation cataract and if so, to estimate the protection factor. Three experiments were carried out. First, two groups of Sprague-Dawley rats were pre-treated with a single application of either placebo or caffeine eye drops in both eyes. All animals were then unilaterally exposed in vivo to 8 kJ/m2 UV-B radiation for 15 min. One week later, the lens GSH levels were measured and the degree of cataract was quantified by measurement of in vitro lens light scattering. In the second experiment, placebo and caffeine pre-treated rats were divided in five UV-B radiation dose groups, receiving 0.0, 2.6, 3.7, 4.5 or 5.2 kJ/m2 UV-B radiation in one eye. Lens light scattering was determined after one week. In the third experiment, placebo and caffeine pre-treated rats were UV-B-exposed and the presence of activated caspase-3 was visualized by immunohistochemistry. There was significantly less UV-B radiation cataract in the caffeine group than in the placebo group (95% confidence interval for mean difference in lens light scattering between the groups = 0.10 ± 0.05 tEDC), and the protection factor for caffeine was 1.23. There was no difference in GSH levels between the placebo- and the caffeine group. There was more caspase-3 staining in UV-B-exposed lenses from the placebo group than in UV-B-exposed lenses from the caffeine group. Topically applied caffeine protects against ultraviolet radiation cataract, reducing lens sensitivity 1.23 times.

In daylight, the human eye is exposed to long wavelength ultraviolet radiation (UVR), visible radiation and short wavelength infrared radiation (IRR). Almost all the UVR and a fraction of the IRR waveband, respectively, left over after attenuation in the cornea, is absorbed in the lens. The time delay between exposure and onset of biological response in the lens varies from immediate-to-short-to-late. After exposure to sunlight or artificial sources, generating irradiances of the same order of magnitude or slightly higher, biological damage may occur photochemically or thermally. Epidemiological studies suggest a dosedependent association between short wavelength UVR and cortical cataract. Experimental data infer that repeated daily in vivo exposures to short wavelength UVR generate photochemically induced damage in the lens, and that short delay onset cataract after UVR exposure is photochemically induced. Epidemiology suggests that daily high-intensity short wavelength IRR exposure of workers, is associated with a higher prevalence of age-related cataract. It cannot be excluded that this effect is owing to a thermally induced higher denaturation rate. Recent experimental data rule out a photochemical effect of 1090 nm in the lens but other wavelengths in the near IRR should be investigated.

ABSTRACT.Purpose: To investigate whether infrared radiation (IRR)-induced cataract is instant or is associated with a time delay between the exposure and the onset of lens light scattering after an exposure to just above threshold dose. Methods: Six-weeks-old albino Sprague-Dawley female rats were unilaterally exposed to 197 W/cm 2 IRR at 1090 nm within the dilated pupil. In the first experiment, the animals were exposed with four exposure times of 5, 8, 13 and 20 second, respectively. At 24 hr after exposure, the light scattering in both exposed and contralateral not exposed lenses was measured. Based on the first experiment, four postexposure time groups were exposed unilaterally to 1090 nm IRR of 197 W/cm 2 for 8 second. At 6, 18, 55 and 168 hr after exposure, the light scattering in both lenses was measured. Results: A 197 W/cm 2 IRR-induced light scattering in the lens with exposures of at least 8 second. Further, after exposure to IRR of 197 W/cm 2 for 8 second, the light-scattering increase in the lens was delayed approximately 16 hr after the exposure. Conclusion: There is a time delay between the exposure and the onset of cataract after exposure to close to threshold dose implicating that either near IRR cataract is photochemical or there is a time delay in the biological expression of thermally induced damage.

Abstract. The damage mechanism for near-infrared radiation (IRR) induced cataract is unclear. Both a photochemical and a thermal mechanism were suggested. The current paper aims to elucidate a photochemical effect based on investigation of irradiance-exposure time reciprocity. Groups of 20 rats were unilaterally exposed to 96-W∕cm 2 IRR at 1090 nm within the dilated pupil accumulating 57, 103, 198, and 344 kJ∕cm 2 , respectively. Temperature was recorded at the limbus of the exposed eye. Seven days after exposure, the lenses were macroscopically imaged and light scattering was quantitatively measured. The average maximum temperature increases for exposure times of 10, 18, 33, and 60 min were expressed as 7.0 AE 1.1, 6.8 AE 1.1, 7.6 AE 1.3, and 7.4 AE 1.1°C [CI (0.95)] at the limbus of the exposed eye. The difference of light scattering in the lenses between exposed and contralateral not-exposed eyes was 0.00 AE 0.02, 0.01 AE 0.03, −0.01 AE 0.02, and −0.01 AE 0.03 transformed equivalent diazepam concentration (tEDC), respectively, and no apparent morphological changes in the lens were observed. An exposure to 96-W∕cm 2 1090-nm IRR projected on the cornea within the dilated pupil accumulating radiant exposures up to 344 kJ∕cm 2 does not induce cataract if the temperature rise at the limbus is <8°C. This is consistent with a thermal damage mechanism for IRR-induced cataract. © The Authors. Published by SPIE under a Creative Commons Attribution 3.0 Unported License. Distribution or reproduction of this work in whole or in part requires full attribution of the original publication, including its DOI.

Close to threshold dose of UVB induces TUNEL-labeling that peaks in the time window 5-120 h after exposure to UVB.