Skip to main content
construction release_alert
Scholars@Duke will be undergoing maintenance April 11-15. Some features may be unavailable during this time.
cancel
Journal cover image

Apolipoprotein E protects against oxidative stress in mixed neuronal-glial cell cultures by reducing glutamate toxicity.

Publication ,  Journal Article
Lee, Y; Aono, M; Laskowitz, D; Warner, DS; Pearlstein, RD
Published in: Neurochem Int
January 2004

Apolipoprotein E (ApoE) deficiency has been shown to adversely affect outcome after transient cerebral ischemia and head trauma. Since oxidative stress contributes to these injuries, the ability of ApoE to reduce irreversible oxidative damage was studied in primary mixed neuronal-glial cell cultures. Cells (13-16 days in vitro) were exposed to 50 microM hydrogen peroxide (H2O2) for 30 min, and toxicity was determined by the release of lactate dehydrogenase (LDH) 24 h after exposure. The presence of recombinant human ApoE2 (100, 300, or 1000 nM) in the culture media partially protected against oxidative injury. This protection was not reversed by pre-treatment with receptor associated protein. The NMDA receptor antagonist, MK-801, also provided partial protection against H2O2 toxicity. The degree of protection was similar to that conferred by ApoE treatment. The protective effects of ApoE and MK-801 were not additive; no ApoE protection was observed in cultures treated with MK-801 prior to H2O2 exposure. ApoE treatment had no effect on H2O2 stimulated glutamate release, but did increase the rate of glutamate uptake via the high affinity glutamate transporter in H2O2 treated cultures. Pre-treatment with ApoE also conferred partial protection against glutamate-induced LDH release. Taken together, these findings suggest that ApoE protects mixed neuronal-glial cell cultures against irreversible oxidative injury from H2O2 by reducing secondary glutamate excitotoxicity.

Duke Scholars

Published In

Neurochem Int

DOI

ISSN

0197-0186

Publication Date

January 2004

Volume

44

Issue

2

Start / End Page

107 / 118

Location

England

Related Subject Headings

  • Rats, Sprague-Dawley
  • Rats
  • Pregnancy
  • Oxidative Stress
  • Oxidants
  • Neurons
  • Neurology & Neurosurgery
  • Neuroglia
  • L-Lactate Dehydrogenase
  • Iron
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Lee, Y., Aono, M., Laskowitz, D., Warner, D. S., & Pearlstein, R. D. (2004). Apolipoprotein E protects against oxidative stress in mixed neuronal-glial cell cultures by reducing glutamate toxicity. Neurochem Int, 44(2), 107–118. https://doi.org/10.1016/s0197-0186(03)00112-8
Lee, Yoonki, Mitsuo Aono, Daniel Laskowitz, David S. Warner, and Robert D. Pearlstein. “Apolipoprotein E protects against oxidative stress in mixed neuronal-glial cell cultures by reducing glutamate toxicity.Neurochem Int 44, no. 2 (January 2004): 107–18. https://doi.org/10.1016/s0197-0186(03)00112-8.
Lee Y, Aono M, Laskowitz D, Warner DS, Pearlstein RD. Apolipoprotein E protects against oxidative stress in mixed neuronal-glial cell cultures by reducing glutamate toxicity. Neurochem Int. 2004 Jan;44(2):107–18.
Lee, Yoonki, et al. “Apolipoprotein E protects against oxidative stress in mixed neuronal-glial cell cultures by reducing glutamate toxicity.Neurochem Int, vol. 44, no. 2, Jan. 2004, pp. 107–18. Pubmed, doi:10.1016/s0197-0186(03)00112-8.
Lee Y, Aono M, Laskowitz D, Warner DS, Pearlstein RD. Apolipoprotein E protects against oxidative stress in mixed neuronal-glial cell cultures by reducing glutamate toxicity. Neurochem Int. 2004 Jan;44(2):107–118.
Journal cover image

Published In

Neurochem Int

DOI

ISSN

0197-0186

Publication Date

January 2004

Volume

44

Issue

2

Start / End Page

107 / 118

Location

England

Related Subject Headings

  • Rats, Sprague-Dawley
  • Rats
  • Pregnancy
  • Oxidative Stress
  • Oxidants
  • Neurons
  • Neurology & Neurosurgery
  • Neuroglia
  • L-Lactate Dehydrogenase
  • Iron