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Retinal macula

Widespread in green leaves fruit e.g. Brassica spp. (Brassicaceae) [leaf], Ananas cosmosus (pineapple) (Bromeliaceae), Vaccinium macrocarpon (Ericaceae), Rheum rhabarbarum (Polygonaceae), Citrus spp. (Rutaceae), Malus, Prunus (Rosaceae) sp. deposited in retinal macula... [Pg.629]

Sensory systems Eyes Vitelliform or egg yolk-like cysts in the retinal macula are typical of Best s disease, an autosomal inherited retinopathy and can also occur in deferoxamine-related retinopathy. This has again been reported in a woman with (unspecified) thalassemia who had been treated with regular blood transfusions and intramuscular and subcutaneous deferoxamine for about 20 years [20 ]. She had bilaterally reduced visual acuity of sudden onset and there were no indicators of a genetic disposition. [Pg.371]

Hahn, P, Milam, AH, and Dunaief, JL, 2003. Maculas affected by age-related macular degeneration contain increased chelatable iron in the retinal pigment epithelium and Bruch s membrane. Arch Ophthalmol 121, 1099-1105. [Pg.343]

Ophthalmologic effects Effects include blurred or diminished vision, scotomata, changes in color vision, corneal deposits, and retinal disturbances, including maculas. [Pg.940]

P-carotene is only one of many antioxidants, which can be detected in the skin. Other carotenoids, for example, lutein and zeaxanthine, are preferentially found in the macula lutea, the so-called yellow spot in the eye. Here, carotenoids are subject to a metabolism typical for that tissue, which cannot be found in other tissues (e.g., formation of meso-zeaxanthine). In addition, they can specifically be absorbed into the macula. In the macula, they protect the retinal pigment epithelial cells against oxidative damage from UV light. Indeed, these two carotenoids can be protective against age-dependent macula degeneration. [Pg.180]

Bone et al.20 originally showed that MP was as highly variable in the infant retina as it is in the adult retina. Z is the dominant carotenoid in the center of the adult retina and L predominates in the periphery (thus, in vivo measures of MP account mostly for zeaxanthin concentration). This ratio appears to be reversed in the infant retina, where L dominates in the center (at this point, of course, the macula is quite immature and similar to the periphery). Although all of the factors responsible for the wide variation in infant MP have not been studied, dietary intake of L and Z is still clearly necessary. Whereas MP can be manipulated in the adult via intake of xanthophyll-rich foods, the obvious concern with infants is that food options are limited to breast milk or manufactured infant formulas. Breast milk contains at least 300 defined nutrients, whereas most infant formulas contain approximately 60-70 defined nutrients76 Currently, infant formula does not contain L and Z in other than trace amounts,76 and many formulas are completely devoid of L. In contrast, breast milk contains L and Z in concentrations that are approximately proportional to maternal intake of these carotenoids.77 These observations are important since many infants are exclusively formula fed. Johnson et al.21 showed that breast-fed infants and formula-fed infants had the same levels of plasma L and Z at birth. After 1 month, however, plasma L and Z significantly increased for the breast-fed infants and decreased in the formula-fed infants. This implies that retinal levels in formula-fed infants are also low. [Pg.98]

Comeal deposits of chloroquine may be asymptomatic or may cause halos around lights or photophobia. These are not a threat to vision and reverse when the dmg is stopped. Retinal toxicity is more serious, however, and may be irreversible. In the early stage it takes the form of visual field defects late retinopathy classically gives the picture of macular pigmentation surrounded by a ring of pigment (the bull s-eye macula). The functional defect can take the form of scotomas, photophobia, defective colour vision and decreased visual acuity resulting, in the extreme case, in blindness. [Pg.272]

A 41-year-old man who had taken vigabatrin for 2 years in doses of 3-6 g/day developed bilateral concentric visual field defects, with greater loss in the nasal fields. Vigabatrin was withdrawn. Later he had a cardiopulmonary arrest and died. At postmortem there was peripheral retinal atrophy with loss of ganghon cells, severe in the peripheral retina and less severe in the maculae. [Pg.3626]

Naturally occurring pigments in the macula limit retinal oxidative damage by absorbing incoming blue... [Pg.74]


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See also in sourсe #XX -- [ Pg.19 , Pg.24 , Pg.32 ]




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