Aluminum impairs glucose utilization and cholinergic activity in rat brain in vitro

Gail V.W. Johnson, Richard S. Jope

Research output: Contribution to journalArticle

58 Scopus citations

Abstract

The effects of AlCl3 on the production of 14CO2 from [U-14C] glucose and high affinity choline transport in rat brain synaptosomes, and on carbachol-stimulated hydrolysis of phosphoinositides in cortical slices were studied. In buffer containing either high K+ (50 mM) or low K+ (4.9 mM), 1 mM AlCl3 significantly depressed the synaptosomal production of 14CO2 from [U-14C]-glucose to 54% and 44% of control rates, respectively. At a concentration of 0.1 mM, AlCl3 depressed the evolution of 14CO2 from [U-14C]glucose from synaptosomes incubated in the high K+ buffer, but did not significantly change 14CO2 production from synaptosomes in the low K+ buffer. Aluminum chloride also inhibited high affinity choline transport in synaptosomes prepared from rat cortex and from hippocampus with an IC50 of approximately 0.5 mM. In brain slices the carbachol-stimulated hydrolysis of phosphoinositides was inhibited by AlCl3 in a dose-dependent manner. One millimolar, 0.5 mM and 0.1 mM AlCl3 inhibited the carbachol-stimulated release of inositol phosphates by 75%, 44% and 33%, respectively. These same concentrations of AlCl3 inhibited the incorporation of [3H] inositol into phospholipids. This inhibitory effect was not dose-dependent as all 3 concentrations of AlCl3 inhibited phospholipid labelling to the same extent (27-37%). These results are discussed in relation to the in vivo neurotoxicity of aluminum.

Original languageEnglish (US)
Pages (from-to)93-102
Number of pages10
JournalToxicology
Volume40
Issue number1
DOIs
StatePublished - Jul 1986
Externally publishedYes

Keywords

  • Aluminum
  • Choline transport
  • Neurotoxin
  • Phosphoinositides

ASJC Scopus subject areas

  • Toxicology

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