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Aluminum Citrate

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R A Yokel – One of the best experts on this subject based on the ideXlab platform.

  • Aluminum Citrate uptake by immortalized brain endothelial cells: implications for its blood-brain barrier transport.
    Brain research, 2002
    Co-Authors: R A Yokel, Marieangela Wilson, Wesley R Harris, Andrew P Halestrap
    Abstract:

    The objective was to further test the hypothesis that Aluminum (Al) Citrate transport across the blood-brain barrier is mediated by a monocarboxylate transporter (MCT). Speciation calculations showed that Al Citrates were the predominant Al species under the conditions employed. Al Citrate did not inhibit lactate uptake and was not taken up by the rat erythrocyte, suggesting it does not serve as an effective substrate for either MCT1 or the anion exchanger. Studies were conducted with b.End5 cells derived from mouse brain endothelial cells to identify the properties of the carrier(s) mediating Al Citrate transport. Western blot analysis of b.End5 cells showed expression of the transferrin receptor and MCT1, but not MCT2 or MCT4. Uptake of Al Citrate was approximately 70% faster than Citrate. Citrate and Al Citrate uptake were sodium independent. Citrate uptake increased at pH 6.9 compared to 7.4, whereas Al Citrate uptake did not. Al Citrate uptake was reduced by inhibitors of mitochondrial respiration and oxidative phosphorylation, suggesting ATP dependence, but not by ouabain, suggesting no role for Na/K-ATPase. Uptake was not affected by alpha-ketoglutarate or malonate, substrates for the dicarboxylate carrier. Many substrates and inhibitors of MCT1 and organic anion transporters reduced Al Citrate uptake into b.End5 cells. BSP and fluorescein, organic anion transporter substrates/inhibitors, inhibited Al Citrate uptake. We conclude that Al Citrate transport across the blood-brain barrier is carrier-mediated, involving either an uncharacterized MCT isoform expressed in the brain such as MCT7 or MCT8 and/or one of the many members of the organic anion transporting protein family, some of which are known to be expressed at the blood-brain barrier.

  • Aluminum Citrate uptake by immortalized brain endothelial cells: implications for its blood-brain barrier transport.
    Brain Research, 2002
    Co-Authors: R A Yokel, Wesley R Harris, Marieangela C. Wilson, Andrew P Halestrap
    Abstract:

    Abstract The objective was to further test the hypothesis that Aluminum (Al) Citrate transport across the blood–brain barrier is mediated by a monocarboxylate transporter (MCT). Speciation calculations showed that Al Citrates were the predominant Al species under the conditions employed. Al Citrate did not inhibit lactate uptake and was not taken up by the rat erythrocyte, suggesting it does not serve as an effective substrate for either MCT1 or the anion exchanger. Studies were conducted with b.End5 cells derived from mouse brain endothelial cells to identify the properties of the carrier(s) mediating Al Citrate transport. Western blot analysis of b.End5 cells showed expression of the transferrin receptor and MCT1, but not MCT2 or MCT4. Uptake of Al Citrate was ∼70% faster than Citrate. Citrate and Al Citrate uptake were sodium independent. Citrate uptake increased at pH 6.9 compared to 7.4, whereas Al Citrate uptake did not. Al Citrate uptake was reduced by inhibitors of mitochondrial respiration and oxidative phosphorylation, suggesting ATP dependence, but not by ouabain, suggesting no role for Na/K-ATPase. Uptake was not affected by α-ketoglutarate or malonate, substrates for the dicarboxylate carrier. Many substrates and inhibitors of MCT1 and organic anion transporters reduced Al Citrate uptake into b.End5 cells. BSP and fluorescein, organic anion transporter substrates/inhibitors, inhibited Al Citrate uptake. We conclude that Al Citrate transport across the blood–brain barrier is carrier-mediated, involving either an uncharacterized MCT isoform expressed in the brain such as MCT7 or MCT8 and/or one of the many members of the organic anion transporting protein family, some of which are known to be expressed at the blood–brain barrier.

  • Research report Aluminum Citrate uptake by immortalized brain endothelial cells: implications for its blood-brain barrier transport
    , 2002
    Co-Authors: R A Yokel, Wesley R Harris, Marieangela C. Wilson, Andrew P Halestrap
    Abstract:

    The objective was to further test the hypothesis that Aluminum (Al) Citrate transport across the blood-brain barrier is mediated by a monocarboxylate transporter (MCT). Speciation calculations showed that Al Citrates were the predominant Al species under the conditions employed. Al Citrate did not inhibit lactate uptake and was not taken up by the rat erythrocyte, suggesting it does not serve as an effective substrate for either MCT1 or the anion exchanger. Studies were conducted with b.End5 cells derived from mouse brain endothelial cells to identify the properties of the carrier(s) mediating Al Citrate transport. Western blot analysis of b.End5 cells showed expression of the transferrin receptor and MCT1, but not MCT2 or MCT4. Uptake of Al Citrate was |70% faster than Citrate. Citrate and Al Citrate uptake were sodium independent. Citrate uptake increased at pH 6.9 compared to 7.4, whereas Al Citrate uptake did not. Al Citrate uptake was reduced by inhibitors of mitochondrial respiration and oxidative phosphorylation, suggesting ATP dependence, but not by ouabain, suggesting no role for Na / K-ATPase. Uptake was not affected by a-ketoglutarate or malonate, substrates for the dicarboxylate carrier. Many substrates and inhibitors of MCT1 and organic anion transporters reduced Al Citrate uptake into b.End5 cells. BSP and fluorescein, organic anion transporter substrates / inhibitors, inhibited Al Citrate uptake. We conclude that Al Citrate transport across the blood-brain barrier is carrier-mediated, involving either an uncharacterized MCT isoform expressed in the brain such as MCT7 or MCT8 and / or one of the many members of the organic anion transporting protein family, some of which are known to be expressed at the blood-brain barrier. © 2002 Elsevier Science B.V. All rights reserved. Theme: Neurotransmitters, modulators, transporters, and receptors Topic: Uptake and transporters

Athanasios Salifoglou – One of the best experts on this subject based on the ideXlab platform.

  • A novel dinuclear species in the aqueous distribution of Aluminum in the presence of Citrate.
    Inorganic chemistry, 2003
    Co-Authors: Maria Dakanali, Catherine P. Raptopoulou, Andrea Lakatos, Tamás Kiss, Aristidis Terzis, István Bányai, Athanasios Salifoglou
    Abstract:

    The chemistry of Aluminum was explored in the presence of the physiological ligand citric acid and in low-pH aqueous media. As a result, the first dinuclear AluminumCitrate complex (NH4)4[Al2(C6H4O7)(C6H5O7)2]·4H2O was isolated at low pH (∼3.5), and was characterized by FT-IR spectroscopy and X-ray crystallography. The structural analysis reveals the presence of a dinuclear assembly of two Aluminum ions octahedrally coordinated to three Citrate ligands of differing protonation state. The NMR solution behavior of this complex emphasizes its time-dependent transformation into a number of variable nature species, ultimately leading to the thermodynamically stable trinuclear species. It also establishes the participation of the dinuclear complex as a viable component of the aqueous Al(III)−Citrate speciation. The chemical and structural features of this novel low molecular mass species provide considerable insight into Citrate‘s ability, as a natural ligand, to influence the chemistry of Aluminum in a pH-dep…

  • Synthesis, Structural Characterization, and Solution Behavior of the First Mononuclear, Aqueous Aluminum Citrate Complex
    Inorganic Chemistry, 1999
    Co-Authors: Manolis Matzapetakis, Catherine P. Raptopoulou, A. Terzis, Andrea Lakatos, Tamás Kiss, Athanasios Salifoglou
    Abstract:

    The significance of the interaction between Aluminum and Citrate in biological media is exemplified by the synthesis, isolation, structural characterization, and solution behavior of the first mononuclear Aluminum Citrate complex. The chemical and structural features of the low molecular weight Aluminum Citrate species characterized help gain insight into Citrate‘s ability, as a natural ligand, to enhance Aluminum‘s absorption and thus affect its accumulation and biotoxicity at biological sites.

Kenneth E Mcmartin – One of the best experts on this subject based on the ideXlab platform.

  • Aluminum Citrate blocks toxicity of calcium oxalate crystals by preventing binding with cell membrane phospholipids.
    American journal of nephrology, 2013
    Co-Authors: Chungang Guo, Tammy R. Dugas, Clinton Scates, Maria Garcia-villarreal, Thomas Ticich, Kenneth E Mcmartin
    Abstract:

    Background/Aims: Renal damage from ethylene glycol and primary hyperoxaluria is linked to accumulation of calcium oxalate monohydrate (COM) crystals in the renal

  • Aluminum Citrate Prevents Renal Injury from Calcium Oxalate Crystal Deposition
    Journal of the American Society of Nephrology : JASN, 2012
    Co-Authors: Lauren M. Besenhofer, Marie C. Cain, Cody L. Dunning, Kenneth E Mcmartin
    Abstract:

    Calcium oxalate monohydrate crystals are responsible for the kidney injury associated with exposure to ethylene glycol or severe hyperoxaluria. Current treatment strategies target the formation of calcium oxalate but not its interaction with kidney tissue. Because Aluminum Citrate blocks calcium oxalate binding and toxicity in human kidney cells, it may provide a different therapeutic approach to calcium oxalate-induced injury. Here, we tested the effects of Aluminum Citrate and sodium Citrate in a Wistar rat model of acute high-dose ethylene glycol exposure. Aluminum Citrate, but not sodium Citrate, attenuated increases in urea nitrogen, creatinine, and the ratio of kidney to body weight in ethylene glycol–treated rats. Compared with ethylene glycol alone, the addition of Aluminum Citrate significantly increased the urinary excretion of both crystalline calcium and crystalline oxalate and decreased the deposition of crystals in renal tissue. In vitro, Aluminum Citrate interacted directly with oxalate crystals to inhibit their uptake by proximal tubule cells. These results suggest that treating with Aluminum Citrate attenuates renal injury in rats with severe ethylene glycol toxicity, apparently by inhibiting calcium oxalate’s interaction with, and retention by, the kidney epithelium.

  • Aluminum Citrate inhibits cytotoxicity and aggregation of oxalate crystals.
    Toxicology, 2006
    Co-Authors: Chungang Guo, Kenneth E Mcmartin
    Abstract:

    Calcium oxalate monohydrate (COM), which represents a major component of kidney stones, is an end metabolite of ethylene glycol. COM accumulation has been linked with acute renal toxicity in ethylene glycol poisoning. COM injures the kidney either by directly producing cytotoxicity to the kidney cells or by aggregating in the kidney lumen leading to the blockage of urine flow. The present studies were designed to examine whether Aluminum Citrate could reduce the toxicity of COM. Toxicity was determined in human proximal tubule cells by leakage of lactate dehydrogenase or uptake of ethidium homodimer and in erythrocytes by degree of hemolysis. Aluminum Citrate significantly inhibited the leakage of lactate dehydrogenase from human proximal tubule cells and protected against cell death from COM. The inhibitory effect of Aluminum Citrate was greater than that of other Citrate or Aluminum salts such as sodium Citrate, Aluminum chloride, calcium Citrate, ammonium Citrate or potassium Citrate. Aluminum Citrate significantly inhibited the aggregation of COM crystals in vitro and decreased red cell membrane damage from COM. Aluminum Citrate appeared to directly interact with COM, but not with the cell membrane. As such, Aluminum Citrate reduced the cytotoxicity by a physico-chemical interaction with the COM surface, and not by dissolving the COM crystals. These studies suggest that Aluminum Citrate may protect against tissue damage that occurs with high levels of oxalate accumulation, especially in ethylene glycol poisoning and possibly in hyperoxaluric states.