Al and Si: their speciation, distribution, and toxicity.
OBJECTIVE
In dialysis patients both aluminum (AI) and silicon (Si) may accumulate. Whereas the toxic effects of AI within this population are clearly established, little is known on the role of Si in the development/protection of particular dialysis-related diseases. A clear insight in the protein binding and speciation of trace elements is important to better understand the mechanisms underlying their toxicity/essentiality. Research in this field however is complex and often prone to analytical difficulties and inaccuracies.


METHODS
In the first part of this review techniques used for speciation studies of AI and Si in biological fluids are discussed. Notwithstanding recent technical advances (a) extraneous metal contamination, (b) unrecognized aspecific binding of metals to proteins, and (c) unwanted interactions with separation equipment such as chromatography columns and ultrafiltration membranes remain important pitfalls and often lead to erroneous conclusions. The factors that determine the speciation of AI and Si and their ultimate tissue distribution and toxicity are dealt with in the second part. Here, experimental data obtained with various speciation techniques are linked to in vivo data on the tissue distribution, localization/toxicity of both elements.


CONCLUSIONS
A model in which the AI tissue distribution/toxicity is mediated by either its citrate or transferrin bound form is proposed.
Department of Nephrology, University of Antwerp, Belgium.
G F
GF
van Landeghem
M E
ME
de Broe
P C
PC
D'Haese
D000535:Aluminum / Q000009:adverse effects* / Q000493:pharmacokinetics* / Q000633:toxicity; D000818:Animals; D006801:Humans; D007676:Kidney Failure, Chronic / Q000628:therapy; D006435:Renal Dialysis / Q000009:adverse effects*; D012825:Silicon / Q000009:adverse effects* / Q000493:pharmacokinetics* / Q000633:toxicity
D000535:Aluminum; D012825:Silicon