Acute toxicity of aluminium to fish eliminated in silicon-rich acid waters

Birchall, J. D.; Exley, Christopher; Chappell, J.S.; Phillips, Michael J.

doi:10.1038/338146a0

Cited by 242 publications

(116 citation statements)

References 12 publications

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“…The formation of dissolved aluminosilicates has been shown to reduce the bioavailability and hence toxicity of Al to fish in controlled experimental exposures (Birchall et al, 1989). The same research group ) also demonstrated that Si could reduce Al toxicity in both a diatom (Navicula pelliculosa) and a green alga (Chlorella vulgaris).…”

Section: Impacts Of Silica On Biological Effects Of Almentioning

confidence: 92%

“…Aluminosilicate formation in these studies was restricted to Si concentrations above ca. 100 to 500 µmol · L -1 , although some evidence suggests aluminosilicate may form at concentrations as low as 40 µmol · L -1 (Birchall et al, 1989). Therefore, this complex may only be significant in waters with relatively high dissolved Si concentrations (e.g., streams), and be of less importance in acidic lakes, which tend to be relatively low in Si (Hutchinson, 1957;Driscoll and Newton, 1985;Findlay and Kasian, 1986;Willén, 1991).…”

Section: Aluminum-silicate Chemical Interactionsmentioning

confidence: 99%

“…Silicon concentrations of 90 µM have been reported for streams (Brown and Driscoll, 1992). Birchall et al (1989) suggested that the formation of hydroxy-aluminosilicate species, enhanced by more alkaline conditions at the gills, blocks the binding or precipitation of Al-OH species at the gills. Recall that we suggested the Al and fulvic acid results of Roy and Campbell (1997) could be explained through a reduction in Al precipitation or polymerization of Al in the more basic gill microenvironment (Section…”

Section: Siliconmentioning

confidence: 99%

“…A 13:1 molar ratio of Si:Al eliminated Al toxicity to 1-g Atlantic salmon fry (170 to, 190 µg · L -1 Al (~7 µM), pH 5, ~50 µM Ca, 96-h exposures; Birchall et al, 1989). Silicon concentrations of 90 µM have been reported for streams (Brown and Driscoll, 1992).…”

Section: Siliconmentioning

confidence: 99%

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The Bioavailability and Toxicity of Aluminum in Aquatic Environments

Gensemer

Playle

1999

Critical Reviews in Environmental Science and Technology

619

435

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ABSTRACT:In this article we review the biological effects of Al, primarily with respect to the chemical factors controlling Al bioavailability and toxicity, and how its biological effects are best predicted. Our intent is not to duplicate recent reviews on Al chemistry or toxicity, but rather to update the literature since these reviews were published, and to focus on Al speciation and other external chemical influences on Al bioavailability to freshwater biota. Briefly, we first review Al chemistry, with a specific focus on understanding, as well as measuring, Al chemical species of importance to aquatic biota. Next we more comprehensively review Al toxicity and bioavailability to freshwater algae, with a thorough analysis of the relationships between speciation and toxicity, the role of important chemical complexing agents such as P, Si, and organic carbon, as well as the potential for Al to impact algal community structure. A third section reviews the more sparse literature on aquatic higher plants; the fourth section reviews a somewhat more abundant literature of Al toxicity to freshwater invertebrates. We close with an updated review of Al toxicity to fish, again with a focus on mechanisms of toxicity, and the role of Al speciation in controlling bioavailability.

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Section: Impacts Of Silica On Biological Effects Of Almentioning

confidence: 92%

Section: Aluminum-silicate Chemical Interactionsmentioning

confidence: 99%

Section: Siliconmentioning

confidence: 99%

Section: Siliconmentioning

confidence: 99%

See 2 more Smart Citations

The Bioavailability and Toxicity of Aluminum in Aquatic Environments

Gensemer

Playle

1999

Critical Reviews in Environmental Science and Technology

619

435

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“…Silicon, in the form of orthosilicic acid [monomeric silicic acid; Si(OH) 4 ], interacts with the alkyl 1,4-diol groups of sugar residues (10) and also with polyhydroxy aluminum (Al), forming hydroxy-aluminosilicate polymers (HAS; ref. 11) and ameliorating Al toxicity (12). Hence, both Al-independent (7) and Al-dependent mechanisms (13) have been proposed for the in vivo action of Si.…”

mentioning

confidence: 99%

Aluminum-dependent regulation of intracellular silicon in the aquatic invertebrate Lymnaea stagnalis

Desouky¹,

Jugdaohsingh²,

McCrohan³

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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Silicon is essential for some plants, diatoms, and sponges but, in higher animals, its endogenous regulation has not been demonstrated. Silicate ions may be natural ligands for aluminum and here we show that, in the freshwater snail (Lymnaea stagnalis), intracellular silicon seems specifically up-regulated in response to sublethal aluminum exposure. X-ray microanalysis showed that exposure of snails to low levels of aluminum led to its accumulation in lysosomal granules, accompanied by marked up-regulation of silicon. Increased lysosomal levels of silicon were a specific response to aluminum because cadmium and zinc had no such effect. Furthermore, intra-lysosomal sulfur from metallothionein and other sulfur-containing ligands was increased after exposure to cadmium and zinc but not aluminum. To ensure that these findings indicated a specific in vivo response, and not ex vivo formation of hydroxy-aluminosilicates (HAS) from added aluminum (555 g͞ liter) and water-borne silicon (43 g͞liter), two further studies were undertaken. In a ligand competition assay the lability of aluminum (527 g͞liter) was completely unaffected by the presence of silicon (46 g͞liter), suggesting the absence of HAS. In addition, exogenous silicon (6.5 mg͞liter), added to the water column to promote formation of HAS, caused a decrease in lysosomal aluminum accumulation, showing that uptake of HAS would not explain the loading of aluminum into lysosomal granules. These findings, and arguments on the stability, lability, and kinetics of aluminum-silicate interactions, suggest that a silicon-specific mechanism exists for the in vivo detoxification of aluminum, which provides regulatory evidence of silicon in a multicellular organism.

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A unifying hypothesis of Alzheimer's disease. III. Risk factors

Heininger

2000

Hum. Psychopharmacol. Clin. Exp.

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Normal ageing and Alzheimer's disease (AD) have many features in common and, in many respects, both conditions only differ by quantitative criteria. A variety of genetic, medical and environmental factors modulate the ageing-related processes leading the brain into the devastation of AD. In accordance with the concept that AD is a metabolic disease, these risk factors deteriorate the homeostasis of the Ca(2+)-energy-redox triangle and disrupt the cerebral reserve capacity under metabolic stress. The major genetic risk factors (APP and presenilin mutations, Down's syndrome, apolipoprotein E4) are associated with a compromise of the homeostatic triangle. The pathophysiological processes leading to this vulnerability remain elusive at present, while mitochondrial mutations can be plausibly integrated into the metabolic scenario. The metabolic leitmotif is particularly evident with medical risk factors which are associated with an impaired cerebral perfusion, such as cerebrovascular diseases including stroke, cardiovascular diseases, hypo- and hypertension. Traumatic brain injury represents another example due to the persistent metabolic stress following the acute event. Thyroid diseases have detrimental sequela for cerebral metabolism as well. Furthermore, major depression and presumably chronic stress endanger susceptible brain areas mediated by a host of hormonal imbalances, particularly the HPA-axis dysregulation. Sociocultural and lifestyle factors like education, physical activity, diet and smoking may also modulate the individual risk affecting both reserve capacity and vulnerability. The pathophysiological relevance of trace metals, including aluminum and iron, is highly controversial; at any rate, they may adversely affect cellular defences, antioxidant competence in particular. The relative contribution of these factors, however, is as individual as the pattern of the factors. In familial AD, the genetic factors clearly drive the sequence of events. A strong interaction of fat metabolism and apoE polymorphism is suggested by intercultural epidemiological findings. In cultures, less plagued by the 'blessings' of the 'cafeteria diet-sedentary' Western lifestyle, apoE4 appears to be not a risk factor for AD. This intriguing evidence suggests that, analogous to cardiovascular diseases, apoE4 requires a hyperlipidaemic lifestyle to manifest as AD risk factor. Overall, the etiology of AD is a key paradigm for a gene-environment interaction. Copyright 2000 John Wiley & Sons, Ltd.

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Acute toxicity of aluminium to fish eliminated in silicon-rich acid waters

Cited by 242 publications

References 12 publications

The Bioavailability and Toxicity of Aluminum in Aquatic Environments

The Bioavailability and Toxicity of Aluminum in Aquatic Environments

Aluminum-dependent regulation of intracellular silicon in the aquatic invertebrate Lymnaea stagnalis

A unifying hypothesis of Alzheimer's disease. III. Risk factors

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