Protective Role of Antioxidants in Eye Health

As with our general health, good nutrition is essential for maintaining healthy vision. As with other diseases discussed in this book, it is the antioxidant nutrients which play a crucial role.

Vitamins A, E and C

For over 60 years, vitamin A has been associated with good eyesight. It is essential for forming the retinal photoreceptor pigments which are the basis of vision. Vitamin A deficiency causes eye tissue to shrink and harden, leading to over-sensitivity to bright light, dry and inflamed eyes and eyelids, and finally to night blindness. Vitamin A deficiency is still the prime cause of child blindness in developing countries. It is also associated with advanced AMD (Seddon et al., 1994).

Seddon et al. (1994) studied the effect of antioxidant supplementation in patients with an advanced form of AMD. In those subjects given a multivitamin-mineral antioxidant supplement containing vitamin E (400 mg day—1), vitamin C (500 mg day—1), selenium (250 ^g day—1) and p-carotene (9 mg day—1), distance visual acuity stabilized over a 18 month period whereas in those given placebo it declined. The supplements successfully halted or reversed the degenerative macular changes in 60% of subjects. This study suggests that vitamins A, C, E and p-carotene have a protective effect in preventing or slowing down the degenerative changes in the macula in early or late stages of AMD.

Carotenoids

Carotenoids have been shown to have a protective role against damaging ultraviolet (UV) light and free radicals. Two carotenoids, lutein and zeaxanthin, are present in relatively high concentrations in the eye and it is thought that they act both as a blue light filter and as antioxidants protecting against free radicals. The best dietary sources of lutein and zeaxanthin are spinach, red peppers, kale, broccoli, peas and celery.

In animals, the formation of drusen in the retina occurs faster in those deprived of carotenoids (Seddon et al., 1994). Similarly, population studies show that people who eat more carotenoid-rich vegetables, particularly those containing lutein and zeaxanthin, have a significantly lower risk of developing AMD (Seddon et al., 1994). Khachik et al. (1997) have concluded from their studies that the proposed oxidative reductive pathways for lutein and zeaxanthin in human retina may therefore play an important role in the prevention of AMD and cataracts. Thus, from these studies it can be concluded that nutritional status plays a vital role in maintaining the functional integrity of the eye.

Zinc

Zinc supplementation has been shown to enhance activity of antioxidant enzymes, notably catalase and SOD (Newsome and Swartz, 1988; Pacifici and Davies, 1991). By this means, zinc inhibits the free radical chain reaction and is known to possess antioxidant properties (Hidalgo et al., 1988; Ophir and Chevian, 1992). Oral administration of zinc induces production of metallothionein to which it binds to form zinc-metallothionein, which is stored in the Ehrlich cells (Krezoski et al., 1988). High concentrations of zinc have been reported in the ocular tissue, especially choroid, retina and RPE (Echert, 1979; Karcioglu, 1982).

Newsome and co-workers (1988) published the results of a double-blind, randomized, placebo-controlled study that investigated the effect of oral zinc supplementation on the natural course of AMD. They reported a significantly lower incidence of visual loss in the treatment group, which also had a lower frequency of exudative lesions during the follow-up period. Stur et al. (1996) reported a 2-year double-blind randomized placebo-controlled study including 112 patients with AMD and choroidal neovascularization, pigment epithelium detachment or both, in one eye, and visual acuity of better than 20/40 and macular degeneration without any exudative lesion in the second eye. It was concluded that oral zinc substitution has no short-term effect on the course of AMD in patients who have an exudative form of the disease in one eye. In our study, 60 patients with AMD and exudative lesions were recruited randomly into two groups (30 patients in each group) (unpublished observations). One group was given 89.5 mg daily of elemental zinc as ZnSO4 and the other group was given placebo. The patients were kept under treatment for 18 months, with follow-up every 3 months and antioxidant status was assessed. It was found that levels of antioxidant enzymes (catalase, SOD and glutathione peroxidase) were increased and lipid peroxidation was decreased significantly. Further studies are being done to correlate the biochemical findings with the clinical outcome of oral zinc supplementation.

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