Aluminium Inhibits Muscarinic Agonist‐Induced Inositol 1,4,5‐Trisphosphate Production and Calcium Mobilization in Permeabilized SH‐SY5Y Human Neuroblastoma Cells

Wood, Peter C.; Wojcikiewicz, Richard J.H.; Burgess, John; Castleden, C. M.; Nahorski, Stefan R.

doi:10.1046/j.1471-4159.1994.62062219.x

Cited by 13 publications

(5 citation statements)

References 20 publications

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“…Acute inhibitory effects of Al on phosphoinositide accumulation and PIP 2 hydrolysis by PI-PLC have been confirmed in a variety of experimental systems: in synaptosomes [111], cortical homogenates [111], hippocampal and cortical slices [103,[111][112][113], neuroblastoma cells [33,56,114], and liposomes [115,116]. Aluminum lactate and aluminum chloride have similar efficacy for inhibiting phosphoinositide accumulation in rat cortical slices [107].…”

Section: Al Inhibits Phosphoinositide Hydrolysis By Pi-plc In Neural mentioning

confidence: 99%

“…Al depresses phosphoinositide hydrolysis by PI-PLC in both agonist-and non-agonist-stimulated phosphoinositide pathways [33,56,104,107,[111][112][113][114]. For example, 10-500 M Al inhibits PIP 2 hydrolysis by PI-PLC in cortical homogenates in a dose-dependent manner with an IC 50 of 100 M [107].…”

Section: Al Inhibits Phosphoinositide Hydrolysis By Pi-plc In Neural mentioning

confidence: 99%

“…Some evidence suggests that Al directly inhibits PI-PLC activity [57,104,111,113,114]. Other evidence suggests Al indirectly inhibits PI-PLC activity by altering PIP 2 availability [29,106,107].…”

Section: Al Inhibits Phosphoinositide Hydrolysis By Pi-plc In Neural mentioning

confidence: 99%

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Aluminum Disruption of Calcium Homeostasis and Signal Transduction Resembles Change that Occurs in Aging and Alzheimer's Disease

Walton

2012

JAD

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Most humans living in industrialized societies are routinely exposed to bioavailable aluminum salts in the form of additives-in commercially-prepared foods, alum-clarified drinking water, certain pharmaceuticals, sunscreens, and other topical applications. Minute amounts of this aluminum are absorbed into the circulation. Trace aluminum levels cross the blood-brain barrier and progressively accumulate in large pyramidal neurons of the hippocampus, cortex, and other brain regions vulnerable in Alzheimer's disease. More aluminum enters the brain than leaves, resulting in a net increase in intraneuronal aluminum with advancing age. Aluminum is responsible for two main types of toxic damage in cells. As a pro-oxidant, aluminum causes oxidative damage both on its own and in synergy with iron. Aluminum also competes with, and substitutes for, essential metals-primarily Mg2+, iron and Ca2+ ions-in or on proteins and their co-factors. The author hypothesizes that intraneuronal aluminum interferes with Ca2+ metabolism in the aged brain and describes a way to test this hypothesis. This paper reviews: 1) major changes that occur in brain Ca2+ homeostasis and Ca2+ signaling, subtly with aging and more overtly in Alzheimer's disease; and 2) evidence from the scientific literature that aluminum causes these same changes in neurons.

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Section: Al Inhibits Phosphoinositide Hydrolysis By Pi-plc In Neural mentioning

confidence: 99%

Section: Al Inhibits Phosphoinositide Hydrolysis By Pi-plc In Neural mentioning

confidence: 99%

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Aluminum Disruption of Calcium Homeostasis and Signal Transduction Resembles Change that Occurs in Aging and Alzheimer's Disease

Walton

2012

JAD

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“…(2) carbachol-induced 1,4,5-triphosphate production and calcium mobilization in SH-SY5Y (neuroblastoma, third generation) cells at the level of 4,5-biphosphate hydrolysis [170]; (3) bradykinin-triggered inositol triphoshate release and change in intracellular Ca 2+ concentrations in neuroblastoma cells also through the protein G/phospholipase C system [171,172]; (4) acetylcholine-stimulated, atropine sensitive Ca 2+ -dependent Cl À current in mouse pancreatic acinar cells by blocking caffeine-sensitive Ca 2+ -induced Ca 2+ mobilization from intracellular pools [173] and (5) phenylephrine-induced repetitive free Ca 2+ transients in rat hepatocytes [174].…”

Section: Neurotransmitter Interaction With Receptorsmentioning

confidence: 99%

Does neurotransmission impairment accompany aluminium neurotoxicity?

Gonçalves

Silva

2007

Journal of Inorganic Biochemistry

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“…(2) Al 3+ disrupts the phosphoinositide and c-AMP signaling pathways and their downstream effects on PKC activity [270,[409][410][411][412][413]. (3) Al 3+ impairs Ca 2+ signaling [313,408,[414][415][416][417][418][419][420][421] and calmodulin-mediated signal transduction [23,178,[422][423][424][425][426][427][428][429][430]. Al 3+ interferes with Ca 2+ signaling by restricting both inositol triphosphate-and caffeine-evoked Ca 2+ release from endoplasmic reticulum stores [313].…”

Section: Calcium Homeostasis and Signaling Are Disrupted In Ad And Chmentioning

confidence: 99%

Chronic Aluminum Intake Causes Alzheimer's Disease: Applying Sir Austin Bradford Hill's Causality Criteria

Walton

2014

JAD

110

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Industrialized societies produce many convenience foods with aluminum additives that enhance various food properties and use alum (aluminum sulfate or aluminum potassium sulfate) in water treatment to enable delivery of large volumes of drinking water to millions of urban consumers. The present causality analysis evaluates the extent to which the routine, life-long intake, and metabolism of aluminum compounds can account for Alzheimer's disease (AD), using Austin Bradford Hill's nine epidemiological and experimental causality criteria, including strength of the relationship, consistency, specificity, temporality, dose-dependent response, biological rationale, coherence with existing knowledge, experimental evidence, and analogy. Mechanisms that underlie the risk of low concentrations of aluminum relate to (1) aluminum's absorption rates, allowing the impression that aluminum is safe to ingest and as an additive in food and drinking water treatment, (2) aluminum's slow progressive uptake into the brain over a long prodromal phase, and (3) aluminum's similarity to iron, in terms of ionic size, allows aluminum to use iron-evolved mechanisms to enter the highly-active, iron-dependent cells responsible for memory processing. Aluminum particularly accumulates in these iron-dependent cells to toxic levels, dysregulating iron homeostasis and causing microtubule depletion, eventually producing changes that result in disconnection of neuronal afferents and efferents, loss of function and regional atrophy consistent with MRI findings in AD brains. AD is a human form of chronic aluminum neurotoxicity. The causality analysis demonstrates that chronic aluminum intake causes AD.

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Aluminium Inhibits Muscarinic Agonist‐Induced Inositol 1,4,5‐Trisphosphate Production and Calcium Mobilization in Permeabilized SH‐SY5Y Human Neuroblastoma Cells

Cited by 13 publications

References 20 publications

Aluminum Disruption of Calcium Homeostasis and Signal Transduction Resembles Change that Occurs in Aging and Alzheimer's Disease

Aluminum Disruption of Calcium Homeostasis and Signal Transduction Resembles Change that Occurs in Aging and Alzheimer's Disease

Does neurotransmission impairment accompany aluminium neurotoxicity?

Chronic Aluminum Intake Causes Alzheimer's Disease: Applying Sir Austin Bradford Hill's Causality Criteria

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