[Is aluminum a cause of Alzheimer's disease?].
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Biomedical subjects
Publications and source records attributed to M Truchet.
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A single injection of a massive dose of Al-gluconate (4 mg.kg-1) into the saphenous vein of the rat did not provoke any ultrastructural damage in the liver cells, from 2 min. to 8 days after the injection. Al hepatocytes overload appeared only in nuclei and not in nuclei and not in lysosomes, contrarily to chronic intoxications. Nuclear Al concentration concerned only a small fraction of the quantity injected; another part was sequestered by the macrophage system after precipitation in the blood as phosphates chemically transformed during their incorporation in lysosomes. This effective detoxication mechanism which functioned probably after a first absorption by the hepatocyte, was likely to depend upon the form of gluconate and would explain the resistance of liver cells.
Bromadiolone damaged the erythrocytes, resulting in a probable saturation of transferrin, a deposit of iron in the connective tissue and in a few cells of the proximal tubules of the kidneys and an increased storage of ferritin in the spleen. In the hepatocytes, mitochondria were distorted, their lipid inclusions being granular; a large depletion of glycogen may be considered a reflection of an elevated phosphorylase a ascribable to the proliferation of the smooth endoplasmic reticulum. In the kidneys, pyelonephritis may be irrelevant to the poisoning of the animals. Bromine could not be detected using microanalytical methods.
Intravenous injections of Al gluconate enhances immediately the aluminium content of the Rat liver. The cell nuclei are mainly involved in Al accumulation which still remains 10 min. After injection. This experimental model of Al overload is of great potential interest to study Al-nucleic acid interactions.
Nephropathic casts are produced in the kidneys of eels adapted to sea water and submitted to Cd exposure. They are made of phosphate and oxalate of calcium and might contain traces of carbonates. Spherites are formed and grow in the lumen of nephrons and collecting tubules; they are linked to a glycoproteic secretion. They are devoid of Cd and do not contribute to excrete the toxic metal.
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Cobalt is specifically detected in ion microanalysis by high mass resolution. This method allows detection of the remaining cobalt in histological sections of Rat's cortex, after treatment by topic application of cobalt powder and demonstrates a diffusion of the metal into the epileptic area.
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Two histophysical methods (electron microprobe and ion microanalyzer) were used on sections of Annelids in order to study the inorganic composition of cement secretory glands. Mg, Ca and P were demonstrated in large amounts in the secretions, associated with organic matter. Traces, or no, Fe, Al and Si were found. Possibilities of artifacts are discussed, and these results are compared with biochemical methods. A hypothesis is proposed in order to explain the differences observed between biochemical and present results, which suggest, for the hardening of cements a different chemical mechanism to that suggested by Vovelle in annelid Sabellaria alveolata.
The presence of aluminium (A1) in the nuclei of thyroid cells (Rabbits), liver and skin cells (Frogs) and in the nucleolus of a Radiolarian is described. The possibilities of artifacts with these two histophysical methods are briefly discussed, and biological significance of this nucleic aluminium is evoked.
EMP and IMA studies show the presence of A1 in the epidermis of larvae and young adults of Discoglossus pictus and Rana esculenta, which disappears during later stages of development. A1 is practically absent in the epidermis of Xenopus laevis and Pleurodeles waltlii. The localization of A1 with EMP and IMA supports the biochemical results. The function of A1 in the epidermis is not known at present.
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