Toxicity aluminium

The metabolism of aluminium in humans. Most is eliminated in the faeces and kidneys, but there is a small accumulation in the whole body, including the brain and lungs. 

However, there is no doubt that aluminium can damage people whose kidney function is impaired. The condition called dialysis dementia was first noticed in patients who had received long-term haemodialysis for renal failure. Its symptoms included speech disorders, memory loss, convulsions and seizures, followed, in some cases, by death within a year. The incidence of the disease was highest when the municipal water used in the dialysis contained high concentrations of aluminium. Aluminium is, therefore, a potential neurotoxin. 

The mechanisms of aluminium toxicity remain uncertain. Here we describe one of several proposals. 

The process is catalysed by an enzyme called hexokinase. Before the ATP can be accepted by the enzyme, it must become complexed to a magnesium ion, Mg +, through oxygen atoms attached to phosphorus atoms 2 and 3 (Structure 9.9). The exact way in which the magnesium ion bridges the two terminal phosphates is 

The change of bridging position is possible because Mg + does not bind particularly strongly to the oxygen donor sites. But suppose substantial amounts of dissolved aluminium are present. 

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W. J. Horst, The role of the apoplast in aluminium toxicity and resistance of higher plants a review. Z. Pjianz.enerndhr. Bodenk. I5S A 9 (1995). 

Aluminium toxicity is a major stress factor in many acidic soils. At soil pH levels below 5.0, intense solubilization of mononuclear A1 species strongly limits root growth by multiple cytotoxic effects mainly on root meristems (240,241). There is increasing evidence that A1 complexation with carboxylates released in apical root zones in response to elevated external Al concentration is a widespread mechanism for Al exclusion in many plant species (Fig. 10). Formation of stable Al complexes occurs with citrate, oxalate, tartarate, and—to a lesser extent— also with malate (86,242,243). The Al carboxylate complexes are less toxic than free ionic Al species (244) and are not taken up by plant roots (240). This explains the well-documented alleviatory effects on root growth in many plant species by carboxylate applications (citric, oxalic, and tartaric acids) to the culture media in presence of toxic Al concentrations (8,244,245) Citrate, malate and oxalate are the carboxylate anions reported so far to be released from Al-stressed plant roots (Fig. 10), and Al resistance of species and cultivars seems to be related to the amount of exuded carboxylates (246,247) but also to the ability to maintain the release of carboxylates over extended periods (248). In contrast to P deficiency-induced carboxylate exudation, which usually increases after several days or weeks of the stress treatment (72,113), exudation of carboxylates in response to Al toxicity is a fast reaction occurring within minutes to several hours... 

Aluminium toxicity is the likely cause of three human disorders arising from long-term haemodialysis vitamin D-resistant osteomalacia, iron adequate microcytic anaemia, and dialysis dementia (Martin, 1994). The first of these conditions is consistent with interference with calcium deposition into bone, and the accumulation of aluminium in the bone matrix. 

Acid sulfate soils are an especially difficult class of acid soil formed in former marine sediments that have been drained. The acidity is generated from the oxidation of pyrite in the soil resulting in acute aluminium toxicity, iron toxicity, and deficiencies of most nutrients, especially phosphate which becomes immobilized in ferric oxide. The development and management of acid sulfate soils are discussed in detail in Dost and van Breemen (1983) and Dent (1986). 

Kidd, P.S. et al.. The role of root exudates in aluminium resistance and silicon-induced amelioration of aluminium toxicity in three varieties of maize Zea mays L.), J. Exp. Bot., 52, 1339, 2001. 

Cocker, K.M., Evans, D.E., and Hobson, M.J., The amelioration of aluminium toxicity by silicon in higher plants solution chemistry or an in planta mechanism Physiol. Plant., 104, 608, 1998. 

Dietrich, D., Schlatter, C., Blau, N. and Fischer, M. (1989). Aluminium and acid rain mitigating effects of NaCl on aluminium toxicity to brown trout (Salmo truttafario) in acid water. Toxicological and Environmental Chemistry 19,17-23. 

Weatherley N. S., Rutt G. P., Thomas S. P., and Ormerod S. J. (1991) Liming acid stream aluminium toxicity to fish in mixing zones. Water Air Soil Pollut. 55, 345-353. 

Acute aluminium toxicity in one reported case followed the introduction of aluminium sulfate (alum) into the urinary tract to treat hemorrhagic cystitis there was apparently both increased absorption, due to the mucosal lesion of the bladder wall, and an increased susceptibility due to pre-existing renal insufficiency (SED-13, 585). 

Aluminium has a close chemical affinity with silicon, which may have a role in protecting against aluminium toxicity (94). Serum aluminium and silicon concentrations were measured in hemodialysis patients from four different centers. Although there was no relation across all centers combined, in one center there was a reciprocal relation in patients on home hemodialysis (who did not require reverse osmosis). Median (range) aluminium concentrations were higher, 2.2 (0.4-9.6) pmol/l when serum silicon was less than 150 pmol/l, and lower, 1.1 (0.2-2.8) pmol/l when serum silicon was greater than 150 pmol/l. In patients treated by hemodialysis without reverse osmosis, high serum silicon concentrations were associated with lower serum aluminium concentrations. Further work is needed to confirm a preventive role for silicon in the accumulation and subsequent toxicity of aluminium in dialysis patients. 

Various authors Research issues in aluminium toxicity. J Toxicol Environ Health (Special Issue) 1996 48 527-686. 

Freunlich M. The spectrum of aluminium toxicity in pediatrics. Int J Pediatr 1988 3 41. 

McCarthy JT, Milliner DS, Johnson WJ. Clinical experience with desferrioxamine in dialysis patients with aluminium toxicity. Q J Med 1990 74(275) 257-76. 

The main hmiting factor in obtaining an optimal response to epoetin is the adequacy of the patient s iron stores (32,33) the response is abated in the presence of iron deficiency, occult blood loss, hemolysis, and other hematological diseases (34,35). Other causes of an inadequate response to epoetin include concurrent infection or inflammatory disease (1), aluminium toxicity, vitamin deficiencies, secondary hyperparathyroidism (36,37), and osteitis fibrosa (38,39). 

Metabolic bone disease in children receiving parenteral nutrition manifests primarily as osteopenia and, on occasion, fractures (5). The etiology is multifactorial calcium and phosphate deficiency play a major role in the preterm infant but the part played by aluminium toxicity in this population is unknown. Lack of reference values of bone histomorphometry in the premature infant, as well as lack of reference data for biochemical markers of bone turnover in these patients, contributes to the uncertainty. Other factors that may play a role in the pathogenesis of bone disease associated with parenteral nutrition include lack of periodic enteral feeding underljdng intestinal disease, including malabsorption and inflammation the presence of neoplasms and drug-induced alterations in calcium and bone metabohsm. However, the true incidence and prevalence of parenteral nutrition-associated bone abnormalities in pediatric patients are unknown. 

Note Sucralfate use can lead to symptoms of aluminium toxicity... 

Hesse, P.R. (1963) Phosphorus relationships in a mangrove-swamp mud with particular reference to aluminium toxicity. Plant and Soil, 19, 205-218. 

Ackrill P, Ralston A], Day JP, et al Successful removal of aluminium from patient with dialysis encephalopathy (letter). Lancet 2 692-693,1980 Altmann P, Hamon C, Blair JA, et al Disturbance of cerebral function by aluminium in haemodialysis patients without overt aluminium toxicity. Lancet 2 7-12,1989 Arieff Al, Cooper JD, Armstrong D, et al Dementia, renal failure, and brain aluminum. Ann Intern Med 90 741-747, 1979... 

Elliott HL, Dryburgh F, Fell GS, et al Aluminium toxicity during regular haemodialysis. BMf 1 1101-1103, 1978... 

Freundlich M, Abitbol C, Zilleruelo G, et al Infant formula as a cause of aluminium toxicity in neonatal uraemia. Lancet 2 527-529,1985... 

Balmey, F.RC. and Nathanson, K. (1977) Relationships between aluminium toxicity and sunflower yields on an Avalon medium sandy loam. Agrochemophysia, 9, 59-66. 

Aluminium is poorly absorbed from the GI tract, which is just as well since antacid preparations used by dyspeptic patients may contain as much as 500 mg of aluminium per tablet. Aluminium levels in water supplies are variable and may contain from less than 50 to more than I0(K) jg/l. This is a potential hazard to renal dialysis patients when the aluminium can enter the body across the dialysis membrane, thus bypassing intestinal absoiption. The water used in dialysis is now treated to remove contaminating metals. Acute aluminium toxicity is extremely rare. Aluminium toxicity in patients with renal dysfunc-... 

Treatment of aluminium toxicity is by prevention. In cases of toxicity, aluminium excretion may be enhanced by using the chelating agent desferrioxamine. 

Aluminium monitoring is of vital importance to patients with chronic renal failure being treated with intermittent hemodialysis. Aluminium sources in these patients are dialysate contamination and the ingestion of aluminium-containing medications. The development of unbiased and precise methods, for the determination of aluminium in biological materials is crucial to monitoring these hemodialysis patients after areas of aluminium toxicity. 

From an environmental standpoint, the recognition that acid rain mobilizes aluminium from poorly buffered soils into the aquatic environment has increased the awareness and concern about aluminium toxicity to aquatic organisms. The acidification of fresh water lakes and rivers in the USA, Canada and particularly the Scandinavian countries, and the subsequent rise in dissolved aluminium levels, has been linked to the decline in fish numbers and, in some cases, to the total elimination of entire fish populations [159,160]. In aquatic systems, it has been demonstrated that the A1(0H)2 species seems to be most toxic to fish [159]. Other workers [161], using thermodynamic calculations in conjunction with fish toxicological experiments, have pointed to the Al(OH) species as also toxic to fish. 

All of the problems outlined above indicate that the production of a synthetic reference water, with well defined total aluminium and Alim content, could prove most useful for aluminium toxicity control in natural waters before a certified natural water sample of well known and stable aluminiiun species content becomes available. 

Kochian, L.V., 1995. Cedular mechanisms of aluminium toxicity and resistance in plants. Annu. Rev. Plant Phys. Plant Mol. Biol. 46, 237-260. 

RufyUdri, G., Declerck, S., Dufey, J.E., Delvaux, B., 2000. Arbuscular mycorrhizal fungi might aUeviate aluminium toxicity in banana plants. New Phytol. 148, 343-352. 

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