Toxic effects of aluminium on nerve cells and synaptic transmission.
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Aluminum↗
Biomedical subjects
E Banin
Publications and source records attributed to E Banin.
Toxic effects of alumino-silicates on nerve cells.
The recently reported presence of alumino-silicates in the core of Alzheimer's senile plaques raises a number of questions concerning the little studied area of interactions between solid particles and neuronal tissue. In this preliminary study we report that contact between crystalline alumino-silicates and cultured neuroblastoma cells selectively caused a rapid increase in membrane electrical conductance and loss of excitable activity. Severe morphological deterioration was subsequently evident within 30 min of exposure. Similar effects were induced by a magnesium silicate mineral but not by aluminum hydroxides or by silicon in the form of quartz. Homogeneously charged synthetic particles did not induce changes in electrical function of the cells. These results suggest that a layout incorporating both negative and positive charges, as can be found on the broken edges of platy clay metallo-silicates, and the non-isodiametrical geometry of the particles may be necessary for the acute neurotoxic interaction observed.
Action Potentials↗
Differentiated neuroblastoma cells are more susceptible to aluminium toxicity than developing cells.
The influence of aluminium (20-50 micrograms/ml) on neuronal function was examined using electrophysiological techniques and neuroblastoma clone cells which offer a convenient model of differentiating and fully active neurons. Two specific questions were addressed: 1) Can differentiated cells maintain their normal excitable function when exposed to aluminium? 2) Can proper development of electrophysiological properties be achieved in its presence? We report that aluminium caused premature onset of deterioration in fully differentiated cells. Within 4-6 days they depolarized from -29.3 +/- 0.9 mV to levels lower than -15 mV; compound polyphasic action potentials were gradually replaced by slow monophasic spikes before the final loss of excitable properties and structural deformations was noticed. Developing cells followed the normal pattern of differentiation in the presence of aluminium: within 7 days they extended neurites, hyperpolarized and exhibited polyphasic spikes. These results show that neuroblastoma cells are apparently less susceptible to aluminium's toxicity during the process of development than after differentiation. Possible mechanisms by which aluminium may exert its effects are discussed in view of these observations.
Aluminum↗
Impaired control of information transfer at an isolated synapse treated by aluminum: is it related to dementia?
Information transfer across an isolated cholinergic synapse exposed to aluminum was investigated using conventional electrophysiological techniques and computer-assisted analysis. Spontaneous and stimulation-induced release of neurotransmitter from frog motor nerve endings was augmented in the presence of aluminum (6-200 micrograms/ml). The release-enhancing effect of aluminum was dose-dependent and it was independent of the concentration of calcium ions in the extracellular solution. These results indicate that aluminum at concentrations similar to those found in the diseased brain of demented patients modulates synaptic transmission.
Acetylcholine↗
Retinitis pigmentosa, Coats disease and uveitis.
PURPOSE: To study the anamnestic immune response to retinal specific antigens of two patients suffering from a rare triad of retinitis pigmentosa, Coats disease and uveitis. PATIENTS: 17-year-old girl presented with an acute episode of panuveitis, and her 19-year-old brother suffered from chronic uveitis. On examination, both patients showed retinal vascular changes and subretinal exudations typical of Coats disease, with bone-spicule pigmentary changes as observed in retinitis pigmentosa. RESULTS: All routine examinations were unrevealing. However, the peripheral lymphocytes from these two siblings gave a specific anamnestic response to retinal antigens in vitro. A stimulation index of 4.6 was obtained when the sister's lymphocytes were stimulated with interphotoreceptor binding protein, IRBP--during the acute stage of the uveitis. The brother's lymphocytes showed a stimulation index of 2.7 towards S-Ag during the chronic phase of his uveitic condition. CONCLUSIONS: These results indicate that autoimmunity towards retinal antigens may play some role in specific types of retinitis pigmentosa. Whether these autoimmune reactions are a primary pathological mechanism or are secondary to the extensive destruction of the photoreceptor layer resulting from the retinitis pigmentosa remains debatable.
Adolescent↗
Aluminum ingestion--is it related to dementia?
Elevated levels of aluminum in brain tissue have been found in demented patients with Alzheimer's disease, with ALS-PD complex of Guam and with dialysis encephalopathy. A possible etiological relationship between enhanced aluminum exposure and impaired mental function was suggested both for ALS-PD of Guam (a region where high contents of aluminum in water are found) and for dialysis encephalopathy which appears in dialyzed patients exposed to high doses of aluminum in medications and in dialysate fluid. The role of aluminum in Alzheimer's disease is not known as is the question of life-long aluminum accumulation in healthy human beings. In this review we have limited ourselves to the issue of oral aluminum ingestion and the possible neurotoxic consequences of such exposure. The following topics are summarized: 1. Physiological mechanisms involved in ingestion and intestinal absorption of aluminum and the influences of pH and available organic complexing agents on these processes. 2. Effects of an aluminum-enriched diet on behavior and on brain metabolism. 3. Dietary sources of aluminum and elevated loads of this substance due to prolonged intake of aluminum-containing medications. The main conclusion of this summary is that aluminum is absorbed and may accumulate in different organs in both adults and infants. Two groups seem to be at particular risk for aluminum related toxicity: people with chronic renal failure treated with aluminum-containing medications and pre-term infants fed on aluminum containing formulate. It seems probable that at least upon short term exposure the healthy human body can defend itself adequately from aluminum's toxic effects. However, not enough information is available on possible effects of life-long exposure to aluminum in the environment, diet and medications, which over decades may lead to accumulation of this substance with expressions of toxicity. Therefore, the question of aluminum's relevance to dementive diseases cannot yet be adequately answered.
Aluminum↗