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M. Neuringer, A. Billingslea, B. Fortune, E.J. Johnson, D.M. Snodderly; Multifocal ERG in monkeys without macular pigment . Invest. Ophthalmol. Vis. Sci. 2004;45(13):5145.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: The dietary xanthophylls lutein (L) and zeaxanthin (Z) are the sources of macular pigment and appear to protect the macula from oxidative and age–related damage. This study examined macular function with the multifocal electroretinogram (mfERG) in rhesus monkeys with a life–long history of dietary xanthophyll exclusion and therefore absence of macular pigment. Methods: From birth to 10–18 yrs of age, 18 rhesus monkeys were fed semipurified diets containing all essential nutrients but no xanthophylls. They had no L or Z in serum or tissues and no macular pigment as measured by two–wavelength reflectometry (ARVO 2001). Twelve then received dietary supplements of pure L (n=6) or pure Z (n=6) at 2.2 mg/kg/day for 6–24 mos, and 6 never received L or Z. Absence of retinal L and Z was confirmed in unsupplemented animals at study conclusion. MfERGs (Veris system, 103 hexagons, unscaled, 200 cd/m2) were recorded after 0 (n=4) or 12–18 mo (n=8) of L or Z supplementation, and in 4 animals both before and after 5 months of supplementation. Response parameters were compared with those from 5 normal age–matched monkeys fed a standard stock diet. Results: Comparisons of all semipurified diet animals with stock diet monkeys found no significant differences in either mfERG amplitudes (scalar product) or latencies (implicit times) of first or second order kernel responses within the macula or in more peripheral retina. Values also did not differ between pre– and post–supplementation recordings. Conclusions: Effects of life–long absence of macular pigment were not detectable with the mfERG. This lack of effect is consistent with our previous findings that the major changes in these animals were in the RPE rather than the neural retina. RPE abnormalities included increases in macular angiographic transmission defects and drusen compared with age–matched normal monkeys (ARVO 2001) and altered profiles of foveal RPE cell density (Leung et al., ARVO 2002).
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