As well prior ocular surgery, a history of ocular inflammation, diabetic retinopathy, myopia, retinal occlusive disease, and rubeosis iridis. We excluded AbMole Povidone iodine patients taking vitamin supplements or other medications which affect trace element concentrations, such as fibrates, carbamazepine, phenytoin and antifolates. Demographical data, medical history and systemic medication are summarized in tables 1 and 2. Age and gender as potentially confounding factors were accounted for by inclusion in the general linear model. In the present study we observed significantly higher levels of cadmium, cobalt, iron, and zinc, while copper levels were reduced in the aqueous humor of patients diagnosed with AMD when compared with patients without AMD. Manganese and selenium levels showed no significant differences between the two groups. After adjustment for multiple testing; cadmium, cobalt, copper and iron remained a significant factor in age- and sex adjusted GLM models for AMD. We are unaware of any previous studies describing trace element concentrations in the aqueous humor of AMD patients, and could not find any respective reference in a computerized search utilizing Medline. There is evidence that oxidative stress is involved in the formation of drusen and in the pathogenesis and progression of AMD. Hydroxyl radicals are extremely reactive, causing lipid peroxidation, DNA strand breaks, and degradation of biomolecules. Particularly in photoreceptors, where there is a high oxygen tension and high concentration of easily oxidized polyunsaturated fatty acids, reactive oxygen species must be tightly controlled to avoid oxidative damage. Oxidative stress and inflammation have both been linked to AMD. In the Fenton reaction, iron reacts with hydrogen peroxide to produce hydroxyl radicals, the most reactive and toxic of the reactive oxygen species. Retinal degeneration has also been observed in hereditary disorders resulting in iron overload, including aceruloplasminemia, hereditary hemochromatosis, pantothenate kinase associated neurodegeneration, and Friedreich��s Ataxia. AMD-affected maculas contained more iron than healthy age-matched maculas 3]. Our results of increased iron in the aqueous humor of AMD patients seem to confirm a role of this metal in the pathogenesis of AMD. Another trace metal known to induce oxidative stress with higher concentration in aqueous humor of AMD patients is cadmium. The biologically significant ionic form of cadmium, Cd2+, binds to many bio-molecules and these interactions underlie the toxicity mechanisms of cadmium. Metallothionein is an important intracellular storage protein for zinc and copper, and its synthesis is decreased in oxidative stress. Considering the tight binding of Cd2+ by metallothionein and the sensitivity of the expression of its genes to stressful conditions, this protein may mediate cadmium toxicity in various ways. These include decrease of the zinc buffering ability of cells in different compartments, changing of the dynamics of zinc exchanges, and decrease of the cellular antioxidant defense. Exposure to cadmium perturbs the homeostasis of other metals, and, reciprocally, this effect depends on the body status of other essential metals such as iron and zinc. This interaction is regularly observed in a variety of conditions. Zinc often affords protection against cadmium toxicity, and cells adapted to high zinc concentrations display changed cellular handling homeostasis of cadmium, manganese, and calcium.