Recent aspects of aluminium chemistry and biology: a survey

摘要

From the time, more than 20 years ago, when Al~(3+) was considered to be toxic and affecting neurological functions―it is so when high doses reach the brain―to today, the advances in understanding the chemistry and in vitro biochemistry of Al~(3+) have been steady and this group of papers reports more gains in our knowledge. It is curious that studies in vivo have yielded very little gain. While one comes away with the general impression that cells have never allowed measurable concentrations of any free Me~(3+) ion to accumulate in them, not just Al~(3+) but Ga~(3+), In~(3+), Cr~(3+), and even Fe~(3+). As free ions―there are many potential binding sites should they gain access to organisms. If the toxicity is fairly general to lipids and proteins then describing it becomes exceedingly difficult. For this reason I missed an account of studies of effects of Al~(3+) on simple cells which can be manipulated in many different ways e.g. using genetics. Turning to therapy, the horny problems of the effects of silicate as a protective agent do not appear to have gained favour. It does seem to be that in most situations, combinations of proteins, especially transferrin, and phosphate and citrate are preferential. Of course silicate may be useful outside organisms to take up Al~(3+) as it does in many minerals. The source of highest organic ligand binding would appear to be phenols as in transferrin, hydroxypyridinone, some ferroxamins and humic acids (note this selectivity is not a choice of 'hard' Al~(3+) interacting with 'hard' acid but is overwhelming due to size selectivity. Al~(3+) is a very small ion and binds best to very small donors e.g. F~- and RO~- (phenolate) rather than -CO_2~-). Clearly, as is true of the study of other metal ions in organisms, much remains to be done to fully appreciate the way Al~(3+) affects living cells and the way in which it can be safely sequestered in higher organisms.