Elsevier

Experimental Eye Research

Volume 83, Issue 6, December 2006, Pages 1493-1504
Experimental Eye Research

Protective effects of soft acrylic yellow filter against blue light-induced retinal damage in rats

https://doi.org/10.1016/j.exer.2006.08.006Get rights and content

Abstract

Recently, a yellow intraocular lens (IOL) was developed for the purpose of reducing potential blue light-induced retinal damage after cataract surgery. However, the effect of yellow filters on retinal protection remains to be clarified. To test the protective effects of yellow filters on blue light-induced retinal damage, a yellow and a clear soft acrylic filter were attached to the right and left eyes, respectively, of albino rats and exposed to 4.5 k lux blue fluorescent lights with peak wavelength at 420 nm (ranging 380–500 nm; short blue) or 446 nm (ranging 400–540 nm; long blue) for 6 h. To assess retinal damage, the electroretinogram (ERG) was recorded at 7 days, outer nuclear layer (ONL) thickness and area were measured at 7 days, apoptosis was analyzed by TUNEL staining at 24 h, and the level of lipid peroxidation in retinas was assessed by Western dot blots using specific antibodies against 4-hydroxynonenal (4-HNE)- and carboxyethylpyrrole (CEP)-modified proteins immediately after light exposure. After short blue light exposure, a- and b-wave ERG amplitudes and the ONL thickness at 1–2.5 mm inferior and 0.5–2.5 mm superior to optic nerve head (ONH) were significantly reduced. TUNEL staining in the ONL at 0–2 mm inferior and 1–2 mm superior to the ONH, and retinal levels of 4-HNE- and CEP-modified proteins were significantly increased in the clear filter-covered eyes compared to yellow filter-covered eyes. After long blue light exposure, the only difference seen was a greater ONL thickness at 1.5 mm superior to the ONH in yellow filter-covered eye. Transmission of light through the yellow filter was 58% for short blue and 89% for long blue compared to the clear filter. The ONL area was not different between clear filter-covered and -uncovered eyes after exposure to short or long blue light. Given the results, yellow IOL material protects the retina against acute shorter wavelength blue light exposure more effectively than the clear IOL material.

Introduction

Epidemiological studies suggest a significant association between exposure to light and the progression and/or severity of age-related macular degeneration (AMD) (Cruickshanks et al., 1993, Tomany et al., 2004) and some forms of retinitis pigmentosa (Cideciyan et al., 1998). In addition, a role for photochemical reactions in the pathogenesis of these diseases has been hypothesized (Meyers et al., 2004). The absorption properties of the cornea and the crystalline lens contribute to the protection of the retina against the hazards of light, i.e., the cornea blocks ultraviolet radiation (UVR) in wavelengths below 300 nm and the crystalline lens blocks UVR between 300 nm and 400 nm (Norren and Vos, 1974). The aging human crystalline lens also blocks potentially phototoxic shorter wavelength blue light (Mellerio, 1987, Bron et al., 2000). The yellowing of the crystalline lens with age is likely attributable to accumulation and aggregation of oxidized or glycosylated lens proteins (Bron et al., 2000), which result in a progressive increase in absorbance within the blue range of visible light (Mellerio, 1987, Weale, 1988).

Removing the crystalline lens by cataract surgery increases the amount of optical radiation that reaches the retina (Mainster and Sparrow, 2003), and implanting an intraocular lens (IOL) can compromise ocular defense against photic retinopathy (Mainster and Sparrow, 2003). IOLs with UVR blocking chromophores bonded to optic polymers were introduced in the early 1980s (Mainster and Sparrow, 2003), and are commonly used in cataract surgery. The transmission properties of the colorless UVR blocking IOLs, however, are not comparable to those of the aging crystalline lens in absorbance of blue light. Recent epidemiological studies suggest that prior cataract surgery, aphakia, and pseudophakia are significant risk factors for late-stage AMD, and that an increase in the amount of shorter wavelength blue light reaching the retina after surgery is speculated to be one of the major causes (Klein et al., 1998, Wang et al., 2003).

To compensate for reduced blue light filtering by the colorless UVR blocking IOLs, blue light- and UVR-absorbing yellow-tinted IOLs were introduced in the 1990s and made with rigid polymethylmethacrylate (PMMA) material (Niwa et al., 1996). More recently, these IOLs were made with foldable silicone or soft acrylic material. However, the protective effects of the yellow IOL filter against light-induced retinal damage in vivo have not been extensively studied (Nilsson et al., 1989).

Previous experimental studies on damaging light exposure in rodent eyes have clarified that light exposure causes photoreceptor cell damage, and that the apoptotic pathway is the main course of light-induced cell death (Wenzel et al., 2005). Intense light exposure causes lipid peroxidation of retinal tissues (Wiegand et al., 1983, Organisciak et al., 1992, Tanito et al., 2006) and oxidative stress is likely to be involved in the pathogenesis of light-induced retinal damage, since the damage caused by light can be reduced by various types of antioxidants (Organisciak et al., 1992, Ranchon et al., 2003, Tanito et al., 2005b, Tanito et al., 2005c, Tomita et al., 2005). Thus, light exposure to rodent eyes is a good model for studying photic retinal injury.

In the current study, we assessed the effects of soft acrylic yellow filters compared to clear soft acrylic filters using blue light-induced retinal damage in albino rats. Two types of blue lamps were tested: one had a shorter (420 nm) peak wavelength and the other one had a longer (446 nm) peak wavelength. Our results indicate that the yellow IOL filter was more effective in protecting retinas morphologically, functionally, and biochemically against shorter wavelength blue light-induced acute retinal damage through its blocking of the transmission of blue light.

Section snippets

Blue fluorescent lamps

Super actinic/03 (TL40W/03) and special blue (F40BB) fluorescent lamps were purchased from Philips Lighting Company (Somerset, NJ). Peak wavelengths of the lamps are 420 nm (short blue light) and 446 nm (long blue light), respectively. The emission spectrum of each lamp was measured by spectrophotometry (USB2000, Ocean Optics, Orlando, FL). Major peak of the spectrum distributes between 380 and 500 nm for the short blue light and between 400 and 540 nm for the long blue light (Fig. 1).

Animal care

All

UV/visible light transmission profiles of the filters and the isolated rat crystalline lens

Transmission profiles of UV/visible light ranging from 300 to 800 nm were recorded using the yellow filter, the clear filter, and the isolated rat crystalline lens (Fig. 3). Both filters completely absorbed light at wavelengths 400 nm and shorter, and transmitted more than 90% of the light at wavelengths 500 nm and longer (Fig. 3A and B). At 420 nm and 446 nm, the clear lens transmitted 72% and 86% of the light, respectively (Fig. 3A), compared to 35% and 60% transmission by the yellow filter (Fig. 3

Discussion

We tested the protective effects of yellow and clear filters against acute light exposure from two sources of blue light, short blue light ranging between 380 and 500 nm and long blue light ranging between 400 and 540 nm (Fig. 1). Since the crystalline lens of rats transmitted stably above 350 nm (Fig. 3C), the results were not influenced by any differential absorption of blue light by the lens. After short blue light exposure, the amplitudes of the a- and b-waves (Fig. 4), the ONL thickness at

Acknowledgments

The authors are grateful to Mark Dittmar (Dean A. McGee Eye Institute) for maintaining the animal colonies used in this study, and to Louisa J. Williams and Linda S. Boone (Dean A. McGee Eye Institute) for their excellent retinal section preparation. This study was supported in part by a research contract from Alcon Laboratories (Fort Worth, TX) and grants from the National Eye Institute (EY04149, EY00871, and EY12190); National Center for Research Resources (RR17703); Research to Prevent

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