@article {4122,
	title = {Intestinal absorption of trace amounts of aluminium in rats studied with (26)aluminium and accelerator mass spectrometry},
	journal = {Clinical Science},
	volume = {92},
	number = {4},
	year = {1997},
	note = {ISI Document Delivery No.: WT732Times Cited: 11Cited Reference Count: 23},
	month = {Apr},
	pages = {379-383},
	type = {Article},
	abstract = {1. Until recently studies of intestinal aluminium absorption used pharmacological amounts of stable Al-27. 2. To examine the intestinal absorption of trace amounts of different chemical compounds of aluminium, in the present study we have employed the long half-life isotope of aluminium, Al-26, and accelerator mass spectrometry, Trace amounts of Al-26 (2.7-12.1ng) as the hydroxide, citrate, citrate plus 1 mmol/kg sodium citrate, or maltolate respectively, were administered to four groups of rats (n = 9 per group) by gavage, Blood and urine samples were collected for 5h and the Al-26 content (as a percentage of the administered dose) determined by accelerator mass spectrometry, 3. The 5h urinary Al-26 excretion amounted to 0.1+/-0.02, 0.7+/-0.2, 5.1+/-1.5 and O.1+/-0.1\% of administered dose in the four groups respectively, There was a strong positive correlation between peak plasma Al-26 (r = 0.98) and urinary Al-26 excretion in individual animals (P<0.001), 4. We conclude that the fractional intestinal absorption of trace oral doses of aluminium hydroxide is at least 0.1\% (compared with the previous estimate of 0.01\% using large Al-27 Oral loads), Absorption of aluminium citrate given alone is significantly greater (0.7\%) and is further increased to 5\% by the accompanying sodium citrate, consistent with an enhancing effect of added citrate upon mucosal aluminium permeability. Aluminium maltolate absorption approximates that of aluminium hydroxide (0.1\%).},
	keywords = {AL-26, aluminium, aluminium citrate, aluminium hydroxide, aluminium maltolate, DIALYSIS ENCEPHALOPATHY, GASTROINTESTINAL ABSORPTION, OSTEODYSTROPHY, sodium citrate},
	isbn = {0143-5221},
	url = {<Go to ISI>://A1997WT73200009},
	author = {Schonholzer, K. W. and Sutton, R. A. L. and Walker, V. R. and Sossi, V. and Schulzer, M. and Orvig, Chris and Venczel, E. and Johnson, R. R. and Vetterli, D. and DittrichHannen, B. and Kubik, P. and Suter, M.}
}
@article {3692,
	title = {Speciation of aluminum in biological systems},
	journal = {Journal of Toxicology and Environmental Health},
	volume = {48},
	number = {6},
	year = {1996},
	note = {ISI Document Delivery No.: VE144Times Cited: 99Cited Reference Count: 131Research Issues in Aluminum Toxicity WorkshopJUL, 1995VANCOUVER, CANADA},
	month = {Aug},
	pages = {543-568},
	type = {Proceedings Paper},
	abstract = {As a {\textquoteright}{\textquoteright}hard{\textquoteright}{\textquoteright} trivalent metal ion, Al3+ binds strongly to oxygen-donor ligands such as citrate and phosphate. The aqueous coordination chemistry of Al is complicated by the tendency of many Al complexes to hydrolyze and form polynuclear species, many of which are sparingly soluble. Thus there is considerable variation among the Al stability constants reported for several important ligands. The complexity in the aqueous chemistry of Al has also affected Al toxicity studies, which have often utilized poorly characterized Al stock solutions. Serum fractionation studies show that most Al is protein bound, primarily to the serum iron transport protein transferrin. Albumin appears to play little, if any, role in serum transport. There is little agreement as to the speciation of the remaining low-molecular-mass fraction of serum Al. The lability of the Al3+ ion precludes the simple separation and identification of individual Al complexes. Computational methods are available for detailed computer calculations of the Al speciation in serum, but efforts in this area have been severely hampered by the uncertainties regarding the stability constants of the low molecular mass Al complexes with Citrate, phosphate, and hydroxide. Specific recommendations for further research on Al speciation include: (1) Determine more accurate Al stability constants with critical low molecular mass ligands such as citrate and phosphate; (2) supplement traditional potentiometric studies on Al complexes with data from other techniques such as Al-27-NMR and accelerator mass spectrometry with Al-26; (3) develop new methods for generating reliable linear free energy relationships for Al complexation; (4) determine equilibrium and rate constants for Al binding to transferrin al 37 degrees C; (5) confirm the possible formation of low-molecular-mass Al-protein complexes following desferrioxamine therapy; (6) continue research efforts to incorporate kinetic considerations into the present equilibrium speciation calculations; (7) improve methods for preparing chemically well-defined stock solutions for toxicological studies; (8) incorporate more detailed speciation data into studies on Al toxicity and pharmacokinetics; and (9) incorporate more detailed speciation data into future epidemiological studies on the relationship between Al toxicity and various water quality parameters.},
	keywords = {ALZHEIMERS-DISEASE, DIETARY CONSTITUENTS, DRINKING-WATER, GASTROINTESTINAL ABSORPTION, HUMAN-SERUM TRANSFERRIN, MURINE, NEUROBLASTOMA-CELLS, POTENTIAL, PROTEIN-BINDING, SIGNIFICANCE INVIVO, SIZE-EXCLUSION CHROMATOGRAPHY, THERAPEUTIC CHELATING-AGENTS},
	isbn = {0098-4108},
	url = {<Go to ISI>://A1996VE14400005},
	author = {Harris, W. R. and Berthon, G. and Day, J. P. and Exley, C. and Flaten, T. P. and Forbes, W. F. and Kiss, T. and Orvig, Chris and Zatta, P. F.}
}
