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 GSK-690693 web tightly controlled to avoid oxidative damage. Oxidative stress and inflammation have both been linked to AMD [8]. In the Fenton reaction, iron reacts with hydrogen peroxide (H2O2) to produce hydroxyl radicals, the most reactive and toxic of the reactive oxygen species (ROS). Retinal degeneration has also been observed in hereditary disorders resulting in iron overload, including aceruloplasminemia, hereditary hemochromatosis, pantothenate kinase associatedneurodegeneration, 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. Some of the molecules specialized in the handling of alkaline earth (Mg2+, Ca2+) and transition metal ions (e.g. Zn2+, Cu2+, Fe3+/2+) should be particularly sensitive to the presence of Cd2+, because they enclose cationic sites to which the toxic metal can bind [12]. Metallothionein is an important intracellular storage protein for zinc and copper, and its synthesis is decreased in oxidative stress [13]. Considering the tight binding of Cd2+ by metallothionein and the sensitivity of the buy GSK343 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 [14]. 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 [15]. Zinc often affords protection against cadmium 1317923 toxicity, and cells adapted to high zinc concentrations display changed cellular handling homeostasis of cadmium, manganese, and calcium [16]. Zinc and copper are cofactors of metalloenzymes that play a critical role in cell structure and function. Among these enzymes is copper-zinc superoxide dismutase, which regulates oxidative stress in the RPE. Studies show that zinc plus copper supplementation decreases the risk of progression of AMD [17]. Aqueous zinc levels were increased while copper concentrations were reduced in our study. A decrease of copper and zinc concentrations in the RPE and choroid complex of AMD-affected subjects has also been reported [18]. It was shown that average levels of zinc and copper in the neural retina were lower in aged eyes than in young eyes, whereas increase in these metal levels occu.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 [8]. In the Fenton reaction, iron reacts with hydrogen peroxide (H2O2) to produce hydroxyl radicals, the most reactive and toxic of the reactive oxygen species (ROS). Retinal degeneration has also been observed in hereditary disorders resulting in iron overload, including aceruloplasminemia, hereditary hemochromatosis, pantothenate kinase associatedneurodegeneration, 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. Some of the molecules specialized in the handling of alkaline earth (Mg2+, Ca2+) and transition metal ions (e.g. Zn2+, Cu2+, Fe3+/2+) should be particularly sensitive to the presence of Cd2+, because they enclose cationic sites to which the toxic metal can bind [12]. Metallothionein is an important intracellular storage protein for zinc and copper, and its synthesis is decreased in oxidative stress [13]. 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 [14]. 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 [15]. Zinc often affords protection against cadmium 1317923 toxicity, and cells adapted to high zinc concentrations display changed cellular handling homeostasis of cadmium, manganese, and calcium [16]. Zinc and copper are cofactors of metalloenzymes that play a critical role in cell structure and function. Among these enzymes is copper-zinc superoxide dismutase, which regulates oxidative stress in the RPE. Studies show that zinc plus copper supplementation decreases the risk of progression of AMD [17]. Aqueous zinc levels were increased while copper concentrations were reduced in our study. A decrease of copper and zinc concentrations in the RPE and choroid complex of AMD-affected subjects has also been reported [18]. It was shown that average levels of zinc and copper in the neural retina were lower in aged eyes than in young eyes, whereas increase in these metal levels occu.
