Aluminium perturbs oscillatory phosphoinositide-mediated calcium signalling in hormone-stimulated hepatocytes

Aluminium is known to be toxic to cells from bone, brain and bone marrow but the molecular target(s) affected by Al3+ are not known. We show here that Al3+ disrupts the oscillatory free Ca2+ responses of hepatocytes exposed to the Ca2(+)-mobilizing agonist phenylephrine. Al3+ initially increases the...

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Bibliographic Details
Published in:Biochemical journal 1990-07, Vol.269 (2), p.547-550
Main Authors: Schöfl, C, Sanchez-Bueno, A, Dixon, C J, Woods, N M, Lee, J A, Cuthbertson, K S, Cobbold, P H, Birchall, J D
Format: Article
Language:English
Subjects:
aluminium
Animals
calcium
Calcium - metabolism
Citrates - pharmacology
Citric Acid
Deferoxamine - pharmacology
Kinetics
Liver - drug effects
Liver - metabolism
Periodicity
Phenylephrine - pharmacology
Phosphatidylinositols - metabolism
Rats
Signal Transduction - drug effects
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Summary:Aluminium is known to be toxic to cells from bone, brain and bone marrow but the molecular target(s) affected by Al3+ are not known. We show here that Al3+ disrupts the oscillatory free Ca2+ responses of hepatocytes exposed to the Ca2(+)-mobilizing agonist phenylephrine. Al3+ initially increases the frequency of the oscillations and later induces broad Ca2+ spikes lasting several minutes. These broad spikes persist after removal of both agonist and Al3+ from the medium. In the absence of agonist, Al3+ has no effect on free Ca2+. The data suggest that some component(s) of the receptor-phosphoinositide-Ca2+ signalling pathway might be the site at which Al3+ exerts toxic effects.
ISSN:0264-6021
1470-8728
DOI:10.1042/bj2690547