Biochemical and Morphological Changes in Rat Lenses after Long-Term UV B Irradiation

To evaluate ocular morphological response to ultraviolet B (UV-B) exposure in guinea pigs fed with normal and low-ascorbic acid (ASA) diets, 24 guinea pigs were randomly divided into UVR (normal diet + UV-B), LVC (low-ASA diet + UV-B) and CTL (normal diet, without UV-B) groups. The irradiated animals were exposed to 8.2 J/cm² of UV-B over 29 weeks. Changes in the cornea and lens were examined using a Scheimpflug camera, specular microscope and histological studies. ASA contents in the plasma, aqueous humor and lens sections were measured by high-performance liquid chromatography. The results showed low contents of ASA in the plasma, aqueous humor and lens sections in LVC. Both irradiated groups displayed corneal epithelial edema, neovascularization in stroma, increase in corneal thickness, decrease in endothelial density, and lens epithelial damage. No significant morphological differences in cornea and lens were found between guinea pigs fed with low-ASA or normal diet.

Section: Discussionsupporting

confidence: 59%

Section: Measurement Of Asamentioning

confidence: 99%

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Ultraviolet B-Induced Corneal and Lens Damage in Guinea Pigs on Low-Ascorbic Acid Diet

Wu¹,

Kojima²,

Shui³

et al. 2004

“…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.…”

Section: Introductionmentioning

confidence: 99%

In vitro UV-B Effect on Lens Protein Solutions

Kojima²,

Shui³

et al. 1997

To investigate the effects of UV-B exposure on the protein solutions of different lens parts, rabbit lenses were separated into the equator (Eq), anterior cortex (Ac), nucleus (Nu) and posterior cortex (Pc). After homogenization, the water-soluble protein from each part was irradiated with UV-B at 0 to 0.225 J/cm². Alterations in the content of protein SH, carbonyl groups, light scattering intensity and SDS-PAGE pattern were measured to compare the effect of UV-B on the protein solutions of various lens parts with or without additional GSH to test its preventive effect. The results showed that after UV-B irradiation, the protein sulfhydryl groups are gradually reduced. The nonprotein thiol (GSH added to the protein solution) was lost more rapidly than the protein sulfhydryl. The high molecular bands on the SDS-PAGE pattern mainly aggregated with disulfide. UV-B damage also increased the content of carbonyl groups and light scattering, irrespective of the lens parts. Lens proteins from the equator suffered the least damage while those of the nucleus were most strongly affected by UV-B exposure. This study suggests that the lens proteins from various lens parts have different responses to UV-B exposure; the sensitivity was in the following order: Eq < Ac ≤ Pc < Nu.

“…UV-B irradiation alone can induce anteri or polar cataract in rat eyes in vivo [4][5][6][7][8]. Hockwin et al [7] reported that when 0.2 J/ cm2 UV-B (every second day) was contin uously administered for more than 5 months, opacity initially appeared in the superficial cortical layer and slowly penetrated into the deeper cortex, approaching the supranuclear layer, and posterior opacity along the posteri or suture was observed.…”

Section: Introductionmentioning

confidence: 99%

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

Hatano

Kojima²

1996

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.