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While we were not the ?rst to coin the term hydroxyalu-minosilicate (HAS), we were the ?rst to demonstrate that the formation of HAS limited the biological availability of aluminum (1). We have since strived to understand as much as we can about the inorganic chemistry of HAS and their role in the biogeochemical cycle of aluminum (2, 3)and through our efforts we have provided a full description of one of the very few examples of the chemistry of silicic acid (4). The latter, in undersaturated solutions (<2.0 mmol/L) at pH below ca 10 is a neutral monomer of which the only known chemistry is (i) with ammonium molybdate to form the Keggin-like molybdosilicic acid complex (the basis for the spectrophotometric measurement of silicic acid) and (ii) with aluminum hydroxide to form HAS. The latter has been shown by us to proceed by a competitive condensation reaction at an hydroxyaluminum surface (4). In a recent paper in Environmental Science & Technology (5) the authors have used the term HAS but they have ascribed their role in limiting the biological availability of aluminum to an alternative reaction pathway involving the reaction of aluminum with polysilicic acids. Many metal cations are chelated by poly-silicic acids (6) and the chemistry is completely different from that of the formation of HAS. The authors should recognize that using the term HAS to describe the products of the reaction of aluminum with polymeric silicic acids is potentially confusing and misleading. In the same paper evidence is presented to support the detoxi?cation of aluminum in the digestive gland in snails by its intralysosomal binding by polymeric silicic acid. The suggestion seems to be that freshwater snails are natural biosilici?ers, capturing silicic acid and concentrating it in lysosomes prior to its deposition as amorphous silica. That freshwater snails deposit amorphous silica is an intriguing suggestion but not one, to my knowledge, that has been supported by experiment or observation. In addition, for such a mechanism to account for the detoxi?cation of aluminum there would need to be a further mechanism for the uptake of aluminum into lysosomes which were actively scavenging and concentrating silicic acid. Again, Occam’s razor would suggest that no such mechanism exists. The limited support provided for such a mechanism in this paper is analyses of a single inorganic particle isolated from a digestive gland of a snail exposed to aluminum. The analyses are qualitative and distinct from other similar analyses published by members of the same research group (7–9)in that there is no evidence of any sulfur. Energy dispersive X-ray spectrometry (EDX) suggested an excess of silicon over aluminum while electron energy loss spectrometry (EELS) showed some similarity with synthetic protoimogolite. There is a simple explanation for this observation. The aggregate in question is a phytolith (amorphous silica of plant/algal origin) which probably originated from the diet of the snail, and upon which are adsorbed HAS. The latter, since aluminum was present in excess of silicic acid in the culture solution, was probably HASA (or protoimogolite) in which the ratio of Si:Al would be ca 0.5 (10), an observation supported by EELS, and could have formed either in the external solution or, conceivably at least, in the digestive gland itself. I am at odds to understand why the authors have chosen to expound a mechanism of detoxi?cation of aluminum in the snail for which there is not, as yet, any scienti?c basis. The authors have shown quite clearly that aluminum is a neurotoxin in the snail and that the toxicity can be alleviated by silicic acid. Upon the basis of the science to-date the mechanism of amelioration is likely to be the same as that described in other biota, which is through the formation of HAS. [ Last edited by syy311 on 2011-3-21 at 16:44 ] |
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