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Toxins copper

These toxic components of the coatings can be copper oxides (I), mercury, tin-bis(tributyl)oxide, barium metaborate, anilide of salicylic acid, phenols and their derivatives, compounds of aminoformic acids, etc. [87]. In the area of metal ion toxins copper protoxide, lead and tin derivatives have recently come into extensive use. [Pg.237]

A spinning molecule on a copper surface and a soccer-ball molecule tethered to a protein may seem no more useful than a spinning ice-skater or a tetherball. Nonetheless, advocates of nanotechnology cite a wealth of potential applications for this new field, including tailored synthetic membranes that can collect specific toxins from industrial waste and computers that process data much faster than today s best models. The list of possible benefits from nanotechnology is limited only by our imaginations. [Pg.572]

Parkinson s disease (PD) is a hypokinetic movement disorder 766 Huntington s disease is a hyperkinetic movement disorder 771 Wilson s disease is a disease of copper accumulation 773 Dystonia is characterized by sustained muscle contractions 775 Many drugs and toxins induce movement disorders 776... [Pg.761]

Rue E, Bmland K (2001) Domoic Acid Binds Iron and Copper a Possible Role for the Toxin Produced by the Marine Diatom Pseudo-nitzschia. Mar Chem 76 127... [Pg.70]

Because 1,4-dichlorobenzene is a liver toxin, it probably can interact with other chemicals that are liver toxicants. These toxicants are many, and include ethanol, halogenated hydrocarbons (chloroform, carbon tetrachloride, etc ), benzene, and other haloalkanes and haloalkenes. In addition, 1,4-dichlorobenzene toxicity may also be exacerbated by concurrent exposure with acetaminophen, heavy metals (copper, iron, arsenic), aflatoxins, pyrrolizidine alkaloids (from some types of plants), high levels of vitamin A, and hepatitis viruses. Such interactions could either be additive or S5mergistic effects. [Pg.152]

Fig. 2. Left Experimental profiles of the conventional DANTE sequence (top) and of the DANTE-Z sequence (bottom). The sample used was 5% H2O in D2O with a tiny amount of copper sulfate added (leading to a T of approximately 3 s). The different traces were obtained by shifting the carrier frequency in 50 Hz steps without readjustment of the spectrometer phase. For each experiment, four scans were acquired in order to perform the complete phase cycling of DANTE-Z. Right (a) The conventional H spectrum of a small protein (toxin 7 60 residues) in D2O at 318 K (b) selection of the aromatic region by the conventional DANTE sequence (c) same as (b) using the DANTE-Z procedure. Experiments were performed at 200 MHz using a routine AC200 Bruker spectrometer. Fig. 2. Left Experimental profiles of the conventional DANTE sequence (top) and of the DANTE-Z sequence (bottom). The sample used was 5% H2O in D2O with a tiny amount of copper sulfate added (leading to a T of approximately 3 s). The different traces were obtained by shifting the carrier frequency in 50 Hz steps without readjustment of the spectrometer phase. For each experiment, four scans were acquired in order to perform the complete phase cycling of DANTE-Z. Right (a) The conventional H spectrum of a small protein (toxin 7 60 residues) in D2O at 318 K (b) selection of the aromatic region by the conventional DANTE sequence (c) same as (b) using the DANTE-Z procedure. Experiments were performed at 200 MHz using a routine AC200 Bruker spectrometer.
The asymmetric synthesis of the spiroazepinone skeleton present in certain marine toxins was reported by Murai et al. A Diels-Alder reaction was key to the synthetic approach. For example, 70 was accessed in 82% yield (96% ee 99 1 exolendo ratio) from 68 and the diene 69 with X = AsF6 in the chiral copper complex (Equation 9) <2002SL403>. [Pg.8]

The discharge of organic pollutants into lakes or declines in the concentrations of copper, zinc, and other heavy metal toxins may promote the growth of phytoplankton (e.g. algal blooms ). Greater biological activity may then increase anoxic conditions in lake bottoms, which stimulate the reductive dissolution of (oxy)(hydr)oxides and increase the mobilization of arsenic. In particular, Martin and Pedersen (2002) concluded that reduced discharges of copper, zinc, and nickel to Balmer Lake, Ontario, Canada, increased phytoplankton production and arsenic mobility in the lake. [Pg.144]

Kartal and Kose (2003) investigated the removal of arsenic from CCA-treated wood with common chelating agents (EDTA, nitrilotriacetic acid (C6H9NO6), and oxalic acid). Dual mixtures of EDTA and oxalic acid and nitrilotriacetic and oxalic acids removed about 100% of the arsenic from sawdust of the wood. However, only about 80 % of the arsenic was removed from wood chips with the same dual solutions. Once the arsenic, copper, chromium, and any other toxins have been removed from the wood, it could be used as a biofuel. [Pg.411]

Rue, E., and Bruland, K. (2001). Domoic acid binds iron and copper A possible role for the toxin produced by the marine diatom Pseudo-nitzschia. Mar. Chem. 76, 127—134. [Pg.1623]

The metabolism of zinc is influenced by hormones, stress situations, lipopolysaccharides, toxins, oxygen radicals, lipid peroxidations, etc. This may lead to fluctuations in the zinc concentration, mainly due to the induction of metallothioneine (MT), which is a transport and intracellular depot protein. One third of this protein consists of cysteine, which binds zinc, copper, cadmium, cobalt and mercury. This protects the body from toxic heavy metal... [Pg.50]

Other chronic disorders cause osteomalacia. " " Phosphate depletion from low dietary intake, phosphate-binding antacids, and oncogenic osteomalacia (potentially phosphaturic effect) can cause osteomalacia. Hypophosphatasia is an inborn error of metabolism in which deficient activity of alkaline phosphatase causes impaired mineralization of bone matrix. Acidosis from renal dysfunction, distal renal tubular acidosis, hypergammaglobulinemic states (e.g., multiple myeloma), and drugs (e.g., chemotherapy) compromises bone mineralization. Renal tubular disorders secondary to Fanconi s syndrome, hereditary diseases (e.g., Wilson s disease, a defect in copper metabolism), acquired disease (e.g., myeloma), and toxins (e.g., lead) cause osteomalacia to varying degrees. Chronic wastage of phosphorus and/or calcium limits mineralization, which may be further compromised by acidosis and secondary hyperparathyroidism. [Pg.1665]

Bile contains a large number of diverse proteins, some resulting from leakage of hepatocellular protein and others derived from plasma (A9, R6). In certain cases, the liver may secrete specific proteins into bile to bind and thus prevent the reabsorption of potential toxins and thus facilitate fecal excretion of these substances (S3). As an example, copper is excreted principally by the biliary route, bound to a carrier protein that prevents intestinal absorption of the biliary copper (G6). The GST can bind a wide range of substances and we have studied the GST content of human bile using material obtained from intact gallbladders following removal at cholecystectomy. [Pg.355]


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See also in sourсe #XX -- [ Pg.101 ]




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