UV-B-lnduced Cataract Model in Brown-Norway Rat Eyes Combined with Preadministration of Buthionine Sulfoximine

Abstract

In order to develop a more adequate ultraviolet (UV)-induced cataract model, a combination of /-buthionine sulfoximine (BSO) treatment was applied to experimental animals. A single administration of BSO 4 mmol/ kg caused reduced glutathione concentration until experimental day 8. In the 0.067-J/cm² UV-B irradiation experiment, the light-scattering intensity of the anterior lens cortex of the combination group was significantly higher than that of the other groups during the second week after irradiation commenced. After the fourth experimental week, however, there was no significant difference between the group treated by UV-B alone and the combination group. In the 0.2-J/cm² UV-B irradiation experiment, anterior polar cataract was seen in the group receiving UV-B alone, as already reported, 6 weeks after starting UV irradiation. Meanwhile, in the combination group, shallow cortical opacity was seen at 26 weeks after the start of experiment in the deeper lenticular layer which was separated from the anterior subcapsular opacity. This anterior shallow cortical opacity seemed to move towards the nuclear region during the time course of the experiment. The results of this experiment suggested that the BSO treatment accelerated cataractogenesis through additional UV-B irradiation. Although more experiments are needed, this model is useful in investigating the connection between UV-B and other cocataractogenic factors in age-related cataract in humans.

In vitro UV-B Effect on Lens Protein Solutions

“…We chose a total dose of UV-B irradiation equal to the single exposure dose that had been used in a rat cata ract model [5], But comparing with a human lens, the intensity of UV-B in the present work was much higher than that which might reach to a human lens [18].…”

“…Ultraviolet B (UV-B) has been considered as a cataractogenesis factor in epidemiological studies and in animal experiments [1][2][3][4][5]. The most probable way that UV-B causes damage to the lens is photooxidation, but details of the mechanisms remain obscure.…”

“…Acute high UV-B radiations in animal models have shown that early opacities occur in the anterior subcapsular cortex of the lens [4,5], However, under the condition of chronic, low-dose, and long-term UV-B irradiation, in the human liv ing eye the cortical opacities appear with much greater frequency in the inferior nasal quadrant [7,8], On the other hand, the de fense system of the lens, such as GSH and superoxide dismutase, which could protect lens components against oxidation, is distrib uted mainly in the outer part of the lens [9][10][11]. These results suggest that UV-B may have a differential influence on different parts of the lens in vivo.…”

Effect of 5-S-GAD on UV-B-induced cataracts in rats

“…Our previous study also showed that total doses of UV-B above 1000 mJ/cm 2 are required to induce cataractogenesis. 7 All rats in this study were exposed to a dose of UV-B once a week, which started at 100 mJ/cm 2 and was gradually increased fi rst to 150 and fi nally to 200 mJ/cm 2 after weekly confi rmation, 1 day before exposure of the absence of corneal opacities by slit-lamp microscopy. The mechanisms of UV-B-induced cataract formation have been speculated to include a number of factors such as production of reactive oxygen species, 18 DNA damage as strand breaks and fragmentation in lens epithelial cells, 19,20 formation of DNA photoproducts, 21 apoptosis 19,20 of lens epithelial cells and subsequent formation of stratifi ed epithelial cells, lower activity of the defense mechanism superoxide dismutase, increment of lipid peroxide, and hypofunction of the capacity to repair damage.…”

“…The light-scattering intensities (LSIs) of the anterior subcapsular and nuclear layers were evaluated using software interfaced with the EAS-1000, which was developed by Sasaki et al 7 Ocular surfaces were examined by slit-lamp microscopy with fl uorescein staining (5 μl, 0.5% solution).…”