PubMed · 5543746
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P Edholm, B Jacobson. 1971-02-04. [Primary contrast equalization].. https://pubmed.ncbi.nlm.nih.gov/5543746/
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Aluminum is extremely common throughout the world and is innocuous under circumneutral or alkaline conditions. However, in acidic environments, it can be a major limiting factor to many plants and aquatic organisms. The greatest concern for toxicity in North America occurs in areas that are affected by wet and dry acid deposition, such as eastern Canada and the northeastern U.S. Acid mine drainage, logging, and water treatment plant effluents containing alum can be other major sources of Al. In solution, the metal can combine with several different agents to affect toxicity. In general, Al hydroxides and monomeric Al are the most toxic forms. Dissolved organic carbons, F, PO(3)3- and SO(4)2- ameliorate toxicity by reducing bioavailability. Elevated metal levels in water and soil can cause serious problems for some plants. Algae tend to be both acid- and Al tolerant and, although some species may disappear with reduced pH, overall algae productivity and biomass are seldom affected if pH is above 3.0. Aluminum and acid toxicity tend to be additive to some algae when pH is less than 4.5. Because the metal binds with inorganic P, it may reduce P availability and reduce productivity. Forest die-backs in North America involving red spruce, Fraser fir, balsam fir, loblolly pine, slash pine, and sugar maples have been ascribed to Al toxicity, and extensive areas of European forests have died because of the combination of high soil Al and low pH. Extensive research on crops has produced Al-resistant cultivars and considerable knowledge about mechanisms of and defenses against toxicity. Very low Al levels may benefit some plants, although the metal is not recognized as an essential nutrient. Hyperaccumulator species of plants may concentrate Al to levels that are toxic to herbivores. Toxicity in aquatic invertebrates is also acid dependent. Taxa such as Ephemeroptera, Plecoptera, and Cladocera are sensitive and may perish when Al is less than 1 mg.L-1 whereas dipterans, molluscs, and isopods seem to be tolerant. In Al-sensitive species, elevated levels (approximately 500 micrograms.L-1) affect ion regulation and respiratory efficiency. Toxicity tends to be greatest near a species' threshold of pH sensitivity. At lower pHs, Al may have a slight ameliorative effect by interfering with H+ transport across membranes. Aquatic invertebrates can accumulate very high levels of Al, but most of this appears to be through adsorption rather than assimilation. Aluminum concentrations may be as high as 5000 mg.kg-1 in insects and greater than 17,000 mg.kg-1 in other invertebrates.(ABSTRACT TRUNCATED AT 400 WORDS)
Several lines of evidence suggest that neurotoxic beta A4 amyloid deposits are of prime importance in the pathogenesis of Alzheimer's disease. Epidemiologically determined risk factors such as Down's syndrome, head injury and apoE allelic status can be explained on the basis of this hypothesis. However, there are difficulties with the hypothesis--amyloid accumulation may be necessary, but is not sufficient to produce the neuronal damage seen in Alzheimer's disease. The association between aluminum exposure and Alzheimer's disease remains unproven and is considered to be increasingly peripheral to recent developments in our understanding of the disease.
In order to develop a clearer understanding of the role of aberrant protein turnover in the pathogenesis of neurodegenerative disorders, the effect of a series of potentially neurotoxic metal ions on a wide range of proteases (lysosomal and cytoplasmic proteinases and peptidases) from human cerebral cortex was determined in vitro. The response of lysosomal and cytoplasmic proteases to inhibition by metal ion species (0.05-5 mmol/l) was broadly similar; Sr2+, Mg2+, Ba2+ or Ca2+ showed little inhibitory effect at any concentration for most protease types, whilst Cu2+, Cd2+, Pb2+, Mg2+ or Zn2+ showed a substantial degree of inhibition, depending on metal ion concentration and enzyme type. Ca2+ activated neutral proteinases were no more susceptible to general metal ion inhibition than most other protease types. Some proteases showed marked activation of activity in the presence of several metal ion species. Both lysosomal and cytoplasmic proteases were relatively insensitive to inhibition by Al3+, compared with that obtained with other metal ion species. It is of note that cathepsin D was particularly resistant to inhibition by most metal ion species, whilst pyroglutamyl aminopeptidase was particularly susceptible to inhibition by low concentrations of many metal ions. The above data suggest that in considering the potential role of neurotoxic metal ions in the pathogenesis of neurodegenerative disorders of the CNS (via protease inhibition in the intracellular protein degradation pathway), attention should be focused on the interactions between a wide range of metal ion species and protease types, rather than be restricted to the Al3+/calpain system (as is presently the case in Alzheimer's disease research). In particular, the potential role of pyroglutamyl aminopeptidase in intracellular protein degradation (in addition to more specialized functions such as neurotransmitter processing) and the pathological consequences of the susceptibility of this enzyme to inhibition by neurotoxic metal ions requires further investigation.