Acrolein, a product of lipid peroxidation, inhibits glucose and glutamate uptake in primary neuronal cultures

Mark A. Lovell, Chengsong Xie, William R. Markesbery

Research output: Contribution to journalArticlepeer-review

110 Scopus citations


Oxidative stress has been implicated in the pathogenesis of several neurodegenerative disorders including Alzheimer's disease (AD). Increased lipid peroxidation, decreased levels of polyunsaturated fatty acids, and increased levels of 4-hydroxynonenal (HNE), F2-isoprostanes, and F4-neuroprostanes are present in the brain in patients with AD. Acrolein, an α,β-unsaturated aldehydic product of lipid peroxidation has been demonstrated to be approximately 100 times more reactive than HNE and is present in neurofibrillary tangles in the brain in AD. We recently demonstrated statistically significant elevated concentrations of extractable acrolein in the hippocampus/parahippocampal gyrus and amygdala in AD compared with age-matched control subjects. Concentrations of acrolein were two to five times those of HNE in the same samples. Treatment of hippocampal cultures with acrolein led to a time- and concentration-dependent decrease in cell survival as well as a concentration-dependent increase in intracellular calcium. In cortical neuron cultures, we now report that acrolein causes a concentration-dependent impairment of glutamate uptake and glucose transport in cortical neuron cultures. Treatment of cortical astrocyte cultures with acrolein led to the same pattern of impairment of glutamate uptake as observed in cortical neuron cultures. Collectively, these data demonstrate neurotoxicity mechanisms of arolein that might be important in the pathogenesis of neuron degeneration in AD. Copyright (C) 2000 Elsevier Science Inc.

Original languageEnglish
Pages (from-to)714-720
Number of pages7
JournalFree Radical Biology and Medicine
Issue number8
StatePublished - Oct 15 2000

Bibliographical note

Funding Information:
Funding for this work was provided by NIH grants 5-P01-AG05119 and 5-P50-AG05144 and by a grant from the Abercrombie Foundation. The authors thank Paula Thomason for editorial and Jane Meara for technical assistance in manuscript preparation.


  • Alzheimer's disease
  • Free radicals
  • Lipid peroxidation
  • Neuronal cultures
  • Neurotoxin

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)


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