PubMed · 4622872
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J C Jones. 1972. Electron beams.. https://pubmed.ncbi.nlm.nih.gov/4622872/
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We determined the influence of aluminum on dendritic transport, using an in vitro system of dissociated mouse hippocampal neurons. Newly synthesized RNA from dissociated mouse hippocampal neurons was more slowly transported into dendrites in the presence of aluminum chloride when compared to those without the addition of aluminum chloride to the culture medium. Suppression of dendritic transport of newly synthesized RNA may be responsible for the dendritic degeneration observed in aluminum neurotoxicity, eventually leading to neuronal degeneration.
The capacity of Al3+-related cations (Sc3+, Ga3+, In3+, Be2+, Y3+, and La3+) to promote membrane rigidification and lateral phase separation was evaluated in liposomes containing zwitterionic (phosphatidylcholine, PC) and negatively charged (phosphatidylserine, PS) phospholipids. These effects were correlated with the capacity of the ions to stimulate Fe2+-supported lipid peroxidation. A13+, Sc3+, Ga3+, In3+, Be2+, Y3+, and La3+ (50-200 microM) increased the order parameter of the fluorescent probe 1,3-diphenylhexatriene incorporated in PC:PS membranes. In addition, the electron paramagnetic resonance spectra of spin-labeled fatty acids indicated a reduction in lipid motion induced by Sc3+, Y3+, and La3+. The effect was found to extend down to carbon 16 on the acyl chain. The ions (10-200 microM) were also able to induce lateral phase separation, as evaluated from the increase in fluorescence quenching of the probe 2-(6-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)dodecanoyl-1-hexadec anoyl-sn-glycero-3-phosphocholine. The ability of the ions to alter membrane lipid packing and induce lateral phase separation correlated in a positive manner (r2 = 0.91 and 0.90, respectively) with their capacity to stimulate the production of Fe2+-initiated 2-thiobarbituric-reactive species, a measure of lipid peroxidation. These results show that Al3+-related metal ions cause membrane rigidification and phase separation, which could affect membrane-related processes. The results support the hypothesis that ions without redox capacity can stimulate Fe2+-initiated lipid peroxidation by increasing lipid packing and by promoting the formation of rigid clusters. Both processes will bring phospholipid acyl chains closer together, thus favoring the propagation step of lipid peroxidation.
The action of aluminum [Al(III)] as Al(acac)3 on erythrocytes causes biophysical effects such as osmotic fragility and echino-acanthocytes formation. In this paper, we present these effects in terms of variation of membrane fluidity, together with findings regarding conformational modifications of membrane proteins consequent to Al(III) exposure, as well as the effects on the mobility of the membrane protein bound sialic acid. To this end, we utilized ESR measurements of rabbits and humans erythrocytic ghosts after probing or labeling with suitable stable radicals used as spin probes or labels. Our results show that the lipophilic, hydrolytically stable toxicant Al(acac)3 causes a remarkable reduction of membrane fluidity in rabbit erythrocytes, an appreciable structural compacting effect on cytoskeletal and transmembrane proteins, as well as a reduction of rotational mobility of cell-surface sialic acid of human erythrocytes.