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At least 19 recordsLinked to original sources
PubMed1988

Tissue distribution of gallium following administration of the gallium-maltol complex in the rat: a model for an aluminium-maltol complex of neurotoxicological interest.

The intestinal absorption and subsequent tissue distribution of aluminium-maltol, a potentially neurotoxic complex found in foods, was investigated using gallium as a marker for aluminium. Gallium or gallium-maltol labelled with 67Ga was administered orally to rats. The amount of gallium in 'blood-free' tissues was measured by correcting for gallium in residual blood and an estimate of intestinal absorption was then made by summing the values for all tissues examined. In both the test (gallium-maltol dosed) and control (gallium only dosed) experiments absorption of gallium was significantly increased in the fasted state when compared with that of the fed animals. In fasted but not in fed animals, administration of gallium-maltol doubled the amount of gallium absorbed when compared with administration of gallium alone.

Aluminum↗
PubMed1986

Comparative pulmonary toxicity of gallium arsenide, gallium(III) oxide, or arsenic(III) oxide intratracheally instilled into rats.

The relative toxicity of gallium arsenide (GaAs) and its metal oxides was assessed by intratracheally instilling particulate suspensions of GaAs (100 mg/kg), equimolar gallium as Ga2O3 (65 mg/kg), or a maximally tolerated nonlethal dose of arsenic as As2O3 (17 mg/kg). Two weeks after dosing, five rats from each group were randomly selected for the biochemical determination of lung lipid, protein, DNA, and collagen (4-hydroxyproline; 4-HP) content. The pulmonary retention of gallium and/or arsenic and the concentration of these metals in blood were also determined. Lungs from the remaining rats (n = 3) were examined histopathologically. Pulmonary exposure to Ga2O3 particulates significantly (p less than 0.05) increased the total lipid content of lungs relative to that observed in the vehicle-treated control animals. This response appeared to be associated with the pulmonary retention of gallium particulates (means = 36% of the gallium dose). In contrast, As2O3 particulates were not retained in the lung. Blood arsenic concentrations were 36 ppm which represented 20% of the total arsenic administered. Treatment with As2O3 significantly elevated lung dry weight as well as protein, DNA, and 4-HP content. These data suggest that As2O3 induced an acute fibrogenic response. The intratracheal instillation of GaAs particulates produced effects similar to those observed with the individual oxides. The total lung content of lipids, protein, and DNA was significantly elevated. These biochemical changes were accompanied by significant increases in lung dry weight and lung wet weight. Lungs from rats receiving GaAs particulates retained 44% of the dose as gallium and 28% of the dose as arsenic at the end of the 14-day study. Blood arsenic concentrations were 44 ppm (7% of the arsenic dose) while gallium was not detected in blood at this time. The primary histopathological observations 14 days after the intratracheal instillation of all metal particulates were an inflammatory response and pneumonocyte hyperplasia. The biological severity of these lesions, in descending order, was GaAs greater than As2O3 much greater than Ga2O3. It must be noted, however, that As2O3 was dosed at 0.25 X moles of GaAs.

Analysis of Variance↗
PubMed1978

The interactions of gallium with various buffers and chelating agents in aqueous solution: gallium-71 and hydrogen-1 NMR studies.

The interactions of gallium (Ga) with the ligands, EDTA, NTA, phosphate, lactate, MOPS, TRIS and HEPES are investigated using both 71Ga and 1H nmr measurements. Both EDTA and NTA form strong complexes with gallium, which have a 1:1 stoichiometry. In alkaline solution the tetrahedral Ga(OD)4- competes strongly with EDTA in complex formation. In the lactate complex, there are probably three lactates per gallium present. The phosphate complexes of gallium are difficult to characterize on the basis of this investigation. The buffers, MOPS, TRIS, and HEPES, do not interact with gallium significantly. The ability of the ligands to bind gallium correlates well with their ability to inhibit gallium incorporation by L1210 leukemic cells.

Buffers↗
PubMed1989

[A basic study on gallium alloys for dental restorations. Improvement of liquid gallium alloy].

This study was made to compare the physical and chemical properties of amalgam with those of gallium alloy in which the invented liquid alloy containing the three fundamental components of Ga-Sn-In or Ga-Sn-In-Ag were used instead of mercury. Experiment 1. The physical and chemical properties were investigated after the liquid gallium alloy and high copper amalgam powder were mixed. The following results were obtained; 1) The invented gallium alloy group showed expansion in dimensional changes immediately after mixing. This alloy group showed the same compressive and diametral tensile strength as those in amalgam after 7 days. 2) This alloy group showed slightly more corrosion weight loss in 0.05% HCl and 1% lactic acid solutions than that in amalgam, but this alloy group showed the same corrosion weight loss in 1% NaCl solution and artificial saliva as in amalgam. Also this alloy group showed more discoloration (delta E, NBS) in 0.1% Na2S solution than that in amalgam, but this showed the same degree of discoloration in artificial saliva. Experiment 2. The physical and chemical properties were investigated after the same liquid gallium alloy and Ag-Pd-Sn-Cu-Zn alloy powder were mixed. The following results were obtained; 1) The invented gallium alloy group showed expansion in dimensional changes immediately after mixing. This showed superior quality in compressive and diametral tensile strength as compared with those of amalgam. 2) The invented gallium alloy showed slightly more corrosion weight loss in 0.05% HCl and 1% lactic acid solutions than that in amalgam, but this alloy group showed the same corrosion weight loss in 1% NaCl solution and artificial saliva as in amalgam. Also this alloy group showed more discoloration (delta E, NBS) in 0.1% solution than that in amalgam, but it was the same in artificial saliva.

Dental Alloys↗
PubMed1977

The gallium melting-point standard: a determination of the liquid-solid equilibrium temperature of pure gallium on the International Practical Temperature Scale of 1968.

The sharpness and reproducibility of the gallium melting point were studied and the melting temperature of gallium in terms of IPTS-68 was determined. Small melting-point cells designed for use with thermistors are described. Nine gallium cells including three levels of purity were used in 68 separate determinations fo the melting point. The melting point of 99.99999% pure gallium in terms of IPTS-68 is found to be 29.771(4) +/- 0.001(4) degree C; the melting range is less than 0.0005 degree C and is reproducible to +/- 0.0004 degree C.

Freezing↗
PubMed1991

Targeting iron-dependent DNA synthesis with gallium and transferrin-gallium.

While iron is essential for numerous intracellular processes, its critical role in DNA synthesis relates to the activity of the iron-containing M2 subunit of ribonucleotide reductase, the enzyme responsible for the synthesis of deoxyribonucleotides. Gallium, a metal which resembles iron with respect to transferrin (Tf) binding, cellular uptake by the Tf receptor and incorporation into ferritin, blocks the cellular uptake of iron and inhibits cell growth. Exposure of HL60 cells to Tf-gallium (Ga) results in decreased deoxyribonucleotide synthesis and a diminution in the electron spin resonance (ESR) spectroscopy signal of ribonucleotide reductase, findings consistent with inhibition of this enzyme. In the present study, Ga nitrate blocked the uptake of 59Fe by L1210 cells and inhibited their proliferation. The ribonucleotide reductase M2 subunit ESR signal in cell cytoplasmic extracts was markedly inhibited in Ga-treated cells; however, the signal was restored to normal within 10 min of exposure of these cytoplasmic extracts to ferrous ammonium sulfate. These results confirm that Ga inhibits DNA synthesis by specifically limiting the amount of intracellular iron needed for the activity of the M2 subunit of ribonucleotide reductase. Further studies utilizing HL60 cells made resistant to Ga showed that these cells were also more resistant to growth inhibition by an anti-Tf receptor monoclonal antibody and deferoxamine. Ga blocks cell growth through inhibition of iron-dependent DNA synthesis. Cells appear to overcome the effects of Ga through compensatory mechanisms involving cellular iron metabolism.

Animals↗
PubMed1992

Gallium-67 distribution in a man with a decrease in both transferrin and hepatic gallium-67 concentration.

A patient with reduced transferrin concentration had a 67Ga scintigram that showed uptake in a peritoneal abscess, pericarditis and pleural effusion but only faint liver uptake. Gallium-67 activity was measured in liver, lung, muscle and plasma samples obtained at autopsy. The percent injected dose/kg for liver and plasma samples was considerably lower than previously reported while that in muscle and lung tissues values were comparable to prior data. In this patient, sites on transferrin available to bind 67Ga were reduced from the normal 40 microM to 5.2 microM; this in turn increased the concentration of radiogallate from 1% to 7%. This elevated free activity increased 67Ga excretion and reduced the amount of 67Ga*transferrin species. These results and those of previous studies suggest that liver uptake is slower than abscess uptake and more sensitive to concentration of 67Ga*transferrin. Iron status is an important facet of the interpretation of 67Ga scintigrams.

Abscess↗
PubMed1990

Gallium-67/stable gadolinium antagonism: MRI contrast agent markedly alters the normal biodistribution of gallium-67.

An 11-yr-old patient was scanned 96 hr after the administration of gallium-67 (67Ga). The scan emulated the biodistribution of a typical bone-seeking radipharmaceutical-rather than that of 67Ga. None of the factors previously identified with alteration of the biodistribution of 67Ga were found. However, the patient had been injected with gadopentetate in conjunction with magnetic resonance imaging 4 hr before receiving the 67Ga. Gadolinium appears to cause a strong carrier-like effect in 67Ga scans.

Burkitt Lymphoma↗
PubMed1990

[Studies on gallium alloys for dental restorations. 2. Electron probe microanalysis for hardened gallium alloys].

Hardened gallium alloys were analyzed by scanning electron microscopy (SEM) and electron probe microanalysis (EPMA). The cores, matrix and white irregular shape phases were visible with SEM. The round or irregular shape cores contained Ag, Pd, Cu and Zn but did not contain Ga and In. The dark irregular shape matrix, which surrounded the core, consisted of Ga-Ag, Ga-Pd, Ga-Cu and Ga-Sn phases. However, the amount of Ga-Sn phase was very low. The white phase in the matrix was Ag-In phase.

Dental Alloys↗
PubMed1978

Studies on gallium accumulation in inflammatory lesions: I. Gallium uptake by human polymorphonuclear leukocytes.

The mechanism of ionic gallium-67 localization in inflammatory lesions was studied. Human polymorphonuclear leukocytes (PMN) had higher Ga-67 uptake than lymphocytes, whereas red blood cells had no affinity for Ga-67. Uptake by PMN showed temperature dependence, was independent of Ga-67 concentrations, and was not inhibited by metabolic inhibitors. However, its binding to PMN could be removed by trypsin but not by neuraminidase. These results are consistent with the hypothesis that the plasma membrane serves as a diffusion barrier and Ga-67 only binds to the surface of the PMN plasma membrane. When this membrane's permeability barrier was disrupted, as in heat-killed PMN, Ga-67 uptake increased markedly. Experimental abscesses were induced with E. coli or turpentine in rabbits. Twenty-four hours after i.v. injection, only 20% of Ga-67 in abscesses was in fractions containing intact PMN, cell debris or bacteria; the remainder was in a soluble, non-cellular fraction (2,500-g supernatant).

Abscess↗
PubMed1979

Studies of gallium accumulation in inflammatory lesions. IV. Kinetics of accumulation and role of polymorphonuclear leukocytes in the distribution of gallium in experimental inflammatory exudates.

The kinetics of 67Ga accumulation in experimental inflammatory exudates were studied. In six rabbits with S. aureus induced abscesses, serial samples of exudate and blood were obtained at 1, 2, 4, 24 and 48 hrs after intravenous injection of 67Ga. The accumulation of 67Ga in the inflammatory exudate was slow with an accumulation half-time of 5.5 hrs. The concentration of 67Ga in the abscesses approached that of blood 48 hrs after injection. Analysis of the distribution of 67Ga in the inflammatory exudate revealed that the portion of 67Ga in the cellular fraction (1,600 xg pellet) correlated best with the number of non-viable polymorphonuclear leukocytes (PMN) (r = 0.81). Its correlation with total number of PMN and bacteria was r = 0.69 and r = 0.35, respectively. Autoradiographic studies confirmed that the majority of 67Ga in the cellular fraction of the exudate was associated with non-viable PMN's.

Animals↗
PubMed1986

Gallium-67 activity in bronchoalveolar lavage fluid in sarcoidosis.

Roentgenograms and gallium-67 scans and gallium-67 counts of BAL fluid samples, together with differential cell counts, have proved to be useful in assessing activity and lung involvement in sarcoidosis. In active pulmonary sarcoidosis gallium-67 scans are usually positive. Quantitation of gallium-67 uptake in lung scans, however, may be difficult. Because gallium-67 uptake and cell counts in BAL fluid may be correlated, we set out to investigate gallium-67 activity in BAL fluid recovered from patient of different groups. Sixteen patients with recently diagnosed and untreated sarcoidosis, nine patients with healthy lungs, and five patients with CFA were studied. Gallium-67 uptake of the lung, gallium-67 activity in the lavage fluid, SACE and LACE levels, and alpha 1-AT activity were measured. Significantly more gallium-67 activity was found in BAL fluid from sarcoidosis patients than in that from CFA patients (alpha = .001) or patients with healthy lungs (alpha = .001). Gallium-67 activity in BAL fluid could be well correlated with the number of lymphocytes in BAL fluid, but poorly with the number of macrophages. Subjects with increased levels of SACE or serum alpha 1-AT showed higher lavage gallium-67 activity than did normals, but no correlation could be established. High gallium-67 activity in lavage fluid may be correlated with acute sarcoidosis or physiological deterioration; low activity denotes change for the better. The results show that gallium-67 counts in BAL fluid reflects the intensity of gallium-67 uptake and thus of activity of pulmonary sarcoidosis.

Bronchi↗