PubMed · 1121045
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W F Bare, N B Jones, E J Middlebrooks. 1975. Algae removal using dissolved air flotation.. https://pubmed.ncbi.nlm.nih.gov/1121045/
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Aluminum is an environmental neurotoxin and a suspected risk factor for Alzheimer's disease. The neurotoxicity of aluminum on cultured neurons of rat cerebral cortex was investigated using an assay system for synapse formation and immunohistochemistry. The frequency of spontaneous oscillations of intracellular Ca2+, which is correlated to the number of synapses, was decreased after exposure to 100 microM of aluminum chloride for 22 days. Long-term application of aluminum (48 days) caused aggregation of cell bodies and fasciculation of processes. Processes and cell bodies were strongly stained by antibody to tau protein, which is one of the main components of Alzheimer's neurofibrillary tangles. It is suggested that the characteristics of the degeneration of cultured neurons induced by aluminum show some similarities to the pathology observed in brains with Alzheimer's disease.
Since aluminum is an extremely difficult element to determine reliably in biological samples, no National Institute of Standards and Technology (NIST) biological standard reference material for tissue has yet been certified for aluminum. A chemical neutron activation analysis procedure employing anion-exchange chromatography was developed. The procedure proved successful in decontaminating radioactivatable sodium and chlorine and phosphorus which can produce aluminum via a fast neutron bombardment. For bovine liver (NIST SRM 1577 a) a value of 2.1 +/- 0.2 micrograms of aluminum/g of sample was determined, comparing favorably to the uncertified value 2 micrograms/g sample. For freeze-dried urine (NIST SRM 2670) a value of 0.18 +/- 0.01 micrograms of aluminum/mL of urine was observed. Its uncertified value is 0.18 micrograms of aluminum/mL of sample. Twenty three individual samples in three different human brains were analyzed for their aluminum content.
Cystic fibrosis (CF) is a genetic disease characterized, in part, by defective regulation of Cl- secretion by airway epithelial cells. In CF, cAMP does not activate Cl- channels in the apical membrane of airway epithelial cells. We report here whole-cell patch-clamp studies demonstrating that pertussis toxin, which uncouples heterotrimeric GTP-binding proteins (G proteins) from their receptors, and guanosine 5'-[beta-thio]diphosphate, which prevents G proteins from interacting with their effectors, increase Cl- currents and restore cAMP-activated Cl- currents in airway epithelial cells isolated from CF patients. In contrast, the G protein activators guanosine 5'-[gamma-thio]triphosphate and AlF4- reduce Cl- currents and inhibit cAMP from activating Cl- currents in normal airway epithelial cells. In CF cells treated with pertussis toxin or guanosine 5'-[beta-thio]diphosphate and in normal cells, cAMP activates a Cl- conductance that has properties similar to CF transmembrane-conductance regulator Cl- channels. We conclude that heterotrimeric G proteins inhibit cAMP-activated Cl- currents in airway epithelial cells and that modulation of the inhibitory G protein signaling pathway may have the therapeutic potential for improving cAMP-activated Cl- secretion in CF.