Transmission of light to the aging human retina: possible implications for age related macular degeneration James Dillon a, * , Lei Zheng a , John C. Merriam a , Elizabeth R. Gaillard b a Department of Ophthalmology, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032, USA b Department of Chemistry and Biochemistry, Northern Illinois University, De Kalb, IL 60115, USA Received 2 March 2004; accepted in revised form 26 June 2004 Available online 13 August 2004 Abstract The purpose of this study is to determine the transmission properties of the anterior segment of the human eye as a function of age and relate those changes to possible consequences for retinal disorders. For this a new method has been developed. This consists of a probe which is inserted into the posterior sclera and detects light passing through the anterior segment. The probe is connected to a CCD spectrophotometer via a fibre optic bundle. Using this, the transmission properties of human cadaver eyes were determined. A young primate anterior segment has a maximum absorption of 365 nm due to the O-beta-glucoside of 3-hydroxykynurenine (3-HKG) in the lens. There is a steep increase in transmission of the human anterior segment at wavelengths longer than 400 nm. With aging there is an increase in absorption throughout the visible such that by the sixth decade only 20% of blue light is transmitted to the retina compared to the young primate eye. The rate of decrease of blue light was similar to the age related change of the ratio of absorbance at 365/320 nm of the lens. (IOVS 41:1454;1999). The age related rate of decrease in the transmission of blue light to the retina was similar to the rate of increase of lipofuscin formation in the retina, and the amount of light absorbed by A2E in the RPE is constant from the second to seventh decade. Although this yellowing is thought to be detrimental to the lens, it would appear to be beneficial to the retina. It was determined that the implantation of a standard IOL after cataract surgery increased the amount of light absorbed by A2-E by approximately a factor of five. q 2004 Elsevier Ltd. All rights reserved. Keywords: spectral sensitivity; ARMD; light damage; human lens; lipofuscin proprietary interest: none 1. Introduction The correlation between increased exposure to light and occurrence of age related macular degeneration (ARMD) is still controversial with little epidemiological evidence for the relationship (Hawkins et al., 1999). However, a correlation between the development of wet ARMD after extracapsular cataract extraction and the implantation of a conventional intra-ocular lens has been recently reported (Pollack et al., 1996). Interestingly, Taylor et al. (1990) suggested an association between the occurrence of ARMD and increased exposure to blue (400–500 nm) and visible (400–700 nm) light. Of fundamental importance to addres- sing this issue is an accurate knowledge of the wavelengths and intensities of light that reach the retina. It is difficult to estimate these quantities and at present the only values available are for the surface of the eye, not the retina. Several native retinal chromophores including melanin (Gurrey et al., 1985), protoporphyrin (Gottsch et al., 1990), retinal (Delmelle, 1978), lipofuscin (Gaillard et al., 1995; Reszka et al., 1995; Wassel, 1999) and the lipofuscin component A2E (Gaillard et al., 1995; Ragauskaite et al., 2001; see below) have been suggested to act as photo- sensitizers of damage. If exposure to light does play a role in the etiology of ARMD, then the absorption spectra of these native chromophores must be considered. Lipofucin, a mixture of chromophores that accumulates in the retinal 0014-4835/$ - see front matter q 2004 Elsevier Ltd. All rights reserved. DOI:10.1016/j.exer.2004.06.025 Experimental Eye Research 79 (2004) 753–759 www.elsevier.com/locate/yexer Abbreviations: CCD, charge coupled device; ARMD, age related macular degeneration; A2-E, 2-(2,6-dimethyl-8-(2,6,6-trimethyl-1-cyclo- hexen-1-yl)-1E,3E,5E,7E-octatetraenyl)-1-(2-hydroxyethyl)-4-(4-methyl- 6-(2,6,6-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E-hexatrienyl-pyridinium; IOL, intraocular lens; RPE, retinal pigment epithelium. * Corresponding author. Dr James Dillion, Department of Ophthal- mology, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032, USA. E-mail address: jpd1@columbia.edu (J. Dillon).