Antioxidant mechanisms in apolipoprotein E deficient mice prior to and following closed head injury

L. Lomnitski, S. Chapman, A. Hochman, R. Kohen, E. Shohami, Y. Chen, V. Trembovler, D. M. Michaelson*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

50 Scopus citations


Apolipoprotein E deficient mice have distinct memory deficits and neurochemical derangements and their recovery from closed head injury is impaired. In the present study, we examined the possibility that the neuronal derangements of apolipoprotein E deficient mice are associated with oxidative stress, which in turn affects their ability to recover from close head injury. It was found that brain phospholipid levels in apolipoprotein E deficient mice are lower than those of the controls (55±15% of control, P<0.01), that the cholesterol levels of the two mice groups are similar and that the levels of conjugated dienes of the apolipoprotein E deficient mice are higher than those of control mice (132±15% of P<0.01). Brains of apolipoprotein E deficient mice had higher Mn-superoxide dismutase (134±7%), catalase (122±8%) and glutathione reductase (167±7%) activities than control (P<0.01), whereas glutathione peroxidase activity and the levels of reduced glutathione and ascorbic acid were similar in the two mouse groups. Closed head injury increased catalase and glutathione peroxidase activities in both mouse groups, whereas glutathione reductase increased only in control mice. The superoxide dismutase activity was unaffected in both groups. These findings suggest that the antioxidative metabolism of apolipoprotein E deficient mice is altered both prior to and following head injury and that antioxidative mechanisms may play a role in mediating the neuronal maintenance and repair derangements of the apolipoprotein E deficient mice. Copyright (C) 1999 Elsevier Science B.V.

Original languageAmerican English
Pages (from-to)359-368
Number of pages10
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Issue number3
StatePublished - 30 Mar 1999

Bibliographical note

Funding Information:
We thank Prof. A. Devir from the Department of Neurobiochemistry, Tel-Aviv University, for her advise and generous help in the lipid analysis. This work was supported in part by grants to DMM from the Fund for Basic Research of the Israel Academy of Sciences (Grant number 670/96), from the United States-Israel Binational Science Foundation (Grant number 95/16), from the Harry Stern National Center for Alzheimer’s Disease, from the Joint German-Israeli Research Programm (Grant 1626) and from the Joseph K. and Inez Eichenbaum Foundation and to LL from the Rubinowicz Fund.


  • Alzheimer's disease
  • Antioxidant
  • Apolipoprotein E
  • Brain
  • Mouse
  • Oxidation stress


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