Objectives: In dialysis patients both aluminum (Al) and silicon (Si) m
ay accumulate. Whereas the toxic effects of Al within this population
are clearly established, little is known on the role of Si in the deve
lopment/protection of particular dialysis-related diseases. A clear in
sight in the protein binding acid speciation of trace elements is impo
rtant to better understand the mechanisms underlying their toxicity/es
sentiality. Research in this field however is complex and often prone
to analytical difficulties and inaccuracies. Design and methods: In th
e first part of this review techniques used for speciation studies of
Al and Si in biological fluids are discussed. Notwithstanding recent t
echnical advances (a) extraneous metal contamination, (b) unrecognized
aspecific binding of metals to proteins, and (c) unwanted interaction
s with separation equipment such as chromatography columns and ultrafi
ltration membranes remain important pitfalls and often lead to erroneo
us conclusions. The factors that determine the speciation of Al and Si
and their ultimate tissue distribution and toxicity are dealt with in
the second part. Here, experimental data obtained with various specia
tion techniques are linked to in vivo data on the tissue distribution,
localization/toxicity of both elements. Conclusions: A model in which
the Al tissue distribution/toxicity is mediated by either its citrate
or transferrin bound form is proposed. Copyright (C) 1998 The Canadia
n Society of Clinical Chemists.