Aluminum intracellular effects

Fluoroaluminate complexes can mimic the action of many hormones, neurotransmitters, and growth factors. G-protein-mediated cell responses are key steps in neurotransmission and intercellular signaling in the brain [20], and TFA acts as an active stimulatory species [21]. Exposure of osteoblasts to TFA results in a marked potentiation of intracellular orthophosphate transport, alluding to the anion s ability to increase bone mineralization [22]. Brief exposure to aluminum fluoride complexes induces prolonged enhancement of synaptic transmission [23] and can potentially affect the activity of many other ion channels and enzymes in the kidney [24]. Rapid and dynamic changes of the cytoskeletal actin network are of vital importance to the motility of many cells, and TFA induction effects a pronounced and sustained... 

Aluminum is reported to stimulate second messenger systems in the absence of F. McDonald and Mamrack (1988) identified an effect of A1 alone on phosphatidylinositol hydrolysis. While the phospholipase C that normally carries out this function is regulated by a G protein, their work involved the purified enzyme with no G-protein component. They found inhibition of hydrolysis of phosphatidylinositol-4,5-bisphosphate, but stimulation of the hydrolysis of phosphatidylinositol. The stimulation should therefore lead to diacylglycerol-dependent increases in intracellular Ca. Their work clearly showed that A1 and not AIF was the active factor, by using F to chelate A1 and reverse the stimulation. 

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