Iron plaque metals

Metal cations in the soil solution may be immobilized by sorption onto iron plaque on root surfaces in submerged soils, in the same way that solubilized Zn + was re-adsorbed on ferric oxide in the experiments in Figure 6.22. Sequestering of metals on the external surfaces of wetland roots in this way limits uptake... 

Reduced to their bare verbal bones, both terms just defined by Pemety prominently appear in one of Duchamp s last ready-mades (MD-196). The immediate function of this minimalist object avant la lettre), inscribed with the artist s monogram M. D., was to serve as a kind of metallic seal set upon the box containing the deluxe edition (32 authorized examples in all) of Robert Lebel s Sur Marcel Duchamp, published the next year to great acclaim. As executed by Duchamp in Paris during the summer of 1958, this is simplicity itself a deep blue, enameled metal (iron) plaque, measuring 15 X 20 cm., which bears an inscription, the kind once familiar to Parisians, neatly laid out in white letters (sans serif). This object, which Jean Clair calls a Ready-made imite, exactly simulates the kind of announcements one formerly saw, a century ago, posted on newly erected apartment buildings. The statement it bears is concise, to say the least ... 

Oxidized root channels have been observed for few species, including rice (0. saliva), cattails, reeds, Spartina sp., Carex sp., and Potomogeton sp. (see review by Mendelssohn et al., 1995). The iron-em-iched plaques essentially consist of FeOOH minerals (Bacha and Hossner, 1977). Iron plaque may be amorphous or crystalline, in the forms of iron such as ferric hydroxides, goethite, lepidocrocite, and siderite. Iron oxides or hydroxides in rhizosphere have high affinity for metals and metalloids. 

In the wetlands of Idaho, the formation of an Fe(III) precipitate (plaque) on the surface of aquatic plant roots (Typha latifolia, cat tail and Phalaris arundinacea, reed canary grass) may provide a means of attenuation and external exclusion of metals and trace elements (Hansel et al, 2002). Iron oxides were predominantly ferrihydrite with lesser amounts of goethite and minor levels of siderite and lepidocrocite. Both spatial and temporal correlations between As and Fe on the root surfaces were observed and arsenic existed as arsenate-iron hydroxide complexes (82%). 

There is considerable evidence that defective homeostasis of redox-active metals, i.e. iron and copper, together with oxidative stress, contributes to the neuropathology of AD. The characteristic histology of AD is the deposition of both Ap, as neurotic plaques (Figure 18.12a), and of the protein tau, as neurofibrillary tangles NFT (Figure 18.12b), predominantly in the cerebral cortex and hippocampus. 

Figure 18.16 Hypothetical model for the metallobiology of AP in Alzheimer s disease. (From Bush, 2003. Copyright 2003, with permission from Elsevier.) The proposed sequence of events (1) concentration of iron and copper increase in the cortex with aging. There is an overproduction of APP and AP in an attempt to suppress cellular metal-ion levels. (2) Hyper-metallation of AP occurs which may facilitate H202 production. (3) Hyper-metallated AP reacts with H202 to generate oxidized and cross-linked forms, which are liberated from the membrane. (4) Soluble AP is released from the membrane and is precipitated by zinc which is released from the synaptic vesicles. Oxidized AP is the major component of the plaque deposits. (5) Oxidized AP initiates microglia activation. (6) H202 crosses cellular membranes to react with Cu and Fe, and generate hydroxyl radicals which oxidize a variety of proteins and lipids.

Cardiovascular heart diseases (CHD) are considered as the clinical expression of advanced atherosclerosis. One of the initial steps in atherogenesis is the oxidative modification of LDL and the uptake of the modified lipoprotein particles by macrophages, which in turn become lipid laden cholesterol-rich cells, so-called foam cells [159]. An accumulation of foam cells in the arterial wall is the first visible sign of atherosclerosis and is termed fatty streak, the precursor to the development of the occlusive plaque [160]. It is well known that oxidation of LDL can be initiated in vitro by incubating isolated LDL particles with cells (macrophages, lymphocytes, smooth muscle cells, or endothelial cells), metal ions (copper or iron), enzymes, oxygen radicals, or UV-light. However less is known about the mechanisms by which... 

The mechanism of AD pathogenesis still remains unclear. However, one mechanism, amyloid (3 (A(3) accumulation, may be due to the disturbance in metal homeostasis in AD brains [Strausak et al., 2001]. A(3 peptides are the major constituents of the amyloid core of senile plaques, which are derived from the amyloid precursor protein (APP) and are secreted into extracelluar spaces. Both APP and A(3 contain a copper-binding domain [Hesse et al., 1994 Atwood et al., 1998]. High concentrations of copper, zinc, and iron have been found within the amyloid deposits in AD brains [Lovell et al., 1998], A(3 peptides can be rapidly precipitated by copper under mildly acidic conditions and by zinc at low physiological (submicromolar) concentrations [Bush et al., 1994], An age-dependent binding between A(3 peptides with excess brain metals (copper, iron, and zinc) induces A(3 peptides to precipitate into metal-enriched plaques [Bush, 2002],... 

Stadler N, Lindner RA, Davies MJ. Direct detection and quantification of transition metal ions in human atherosclerotic plaques evidence for the presence of elevated levels of iron and copper. Arterioscler Thromb Vase Biol 2004 24(5) 949-954. 

The other important source of free radicals comes from redox-active metals. Strikingly, NFT and A() plaques were found coincident with overaccumulation of iron in the hippocampus, cerebral cortex, and basal nucleus of Meynert (Lovell et al.,... 

Zinc (Zn +) is the second most abundant metal ion after iron in the human body, and plays critical roles in regulating gene expression, enzyme regulation, and neurotransmission [90]. Zn + is also known to be responsible for the formation of amyloid plaques during the onset of Alzheimer s disease [91], At present, there is considerable interest in the development of Zn +-selective luminescence chemosensors as bioimaging probes [92, 93],... 

The metal ion homeostasis is severely deregulated in Alzheimer s disease (Ehmann et al. 1986, Thompson etal. 1988, Samudralwar etal. 1995, Deibel et al. 1996, Cornett et al. 1998, Lovell et al. 1998). Increased concentrations of copper, iron, and zinc were detected in the neuropil of the brain where they were highly concentrated within amyloid plaques and reached concentrations up to 0.4 (jM (Cu) and 1 fM (Fe and Zn) (Smith et al. 1997, Lovell 1998). A hkely reason is that Ap binds equimolar amounts of Cu(II) and Zn(II) at pH 7.4 (Bush et al. 1993, 1994, Huang et al. 1997, Atwood et al. 1998). The amyloid precursor protein is a transmembrane glycoprotein that undergoes extensive alternative sphcing (Sandbrink etal. 1994) and has been shown to bind Zn(II) and Cu(II) at two distinc sites (Bush etal. 1993, Hesse etal. 1994). Experimentally induced disturbances of the homeostasis of Zn(II) and Cu(II) affect the metabo-hsm of the amyloid precursor protein (Borchardt et al. 1999, 2000). 

An elucidation of the mechanisms of brain iron homeostasis, as outlined in figure 1, will help our understanding of AD especially since iron binds to Ap-peptide and enhances beta-amyloid toxicity [35-38]. Excess iron accumulation is a consistent observation in the AD brain. As discussed above, patients with hemochromatosis are at risk developing AD at an earlier age [2]. Brain autopsy samples from AD patients have elevated levels of ferritin iron, particularly in the neurons of the basal ganglia [39] and most amyloid plaques contain iron and ferritin-rich cells [40]. Clinically there is a reported decrease in the rate of decline in AD patients who were treated with the intramuscular iron chelator, desferrioxamine [41]. Iron enhances cleavage of the Ap-peptide domain of APP by the metalloprotease alpha secretase [42, 43]. Part of the protective effect of the major cleavage product of APP, APP(s), may derive from its capacity to scavange metals to diminish metal-catalyzed oxidative stress to neuronal cells [44]. APP is, itself, a metalloprotein [4]. 

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