Selenium biochemistry is reviewed in respect to its presumed relevance to age-related ocular diseases. Selenium is an essential trace element that exerts its physiological role as selenocysteine residue in at least 25 distinct selenoenzymes in mammals. Lack of GPx-1 due to alimentary selenium deprivation has been inferred to induce cataract in rats and was demonstrated to cause cataracts in mice by targeted gene disruption. The role of other selenoproteins in the eye remains to be worked out. Selenium in excess of the tiny amounts required for selenoprotein synthesis is toxic in general and causes cataracts in experimental animals. Clinical evidence for a protective role of selenium in the development of cataract, macula degeneration, retinitis pigmentosa or any other ocular disease is not available, likely because suboptimum selenium intake, as it may result from unbalanced diet, does not cause any pathologically relevant selenium deficiency in the eye. At present, there is neither theoretical nor an empirical basis to expect beneficial effects of selenium supplementation beyond the dietary reference intakes of 55 microg/day in the context of ocular diseases.