Apolipoprotein E expression and behavioral toxicity of high charge, high energy (HZE) particle radiation.

Published

Journal Article

UNLABELLED: Apolipoprotein E (apoE) is a lipid binding protein that plays an important role in tissue repair following brain injury. In the present studies, we have investigated whether apoE affects the behavioral toxicity of high charge, high energy (HZE) particle radiation. METHODS: Sixteen male apoE knockout (KO) mice and sixteen genetically matched wild-type (WT) C57BL mice were used in this experiment. Half of the KO and half of the WT animals were irradiated with 600 MeV/amu iron particles (2 Gy whole body). The effect of irradiation on motor coordination and stamina (Rotarod test), exploratory behavior (open field test), and spatial working and reference memory (Morris water maze) was assessed. ROTAROD TEST: Performance was adversely affected by radiation exposure in both KO and WT groups at 30 d after irradiation. By 60 d after radiation, the radiation effect was lost in WT, but still apparent in irradiated KO mice. OPEN FIELD TEST: Radiation reduced open field exploratory activity 14, 28, 56, 84, and 168 d after irradiation of KO mice, but had no effect on WT mice. MORRIS WATER MAZE: Radiation adversely affected spatial working memory in the KO mice, but had no discernible effect in the WT mice as assessed 180 d after irradiation. In contrast, irradiated WT mice showed marked impairment of spatial reference memory in comparison to non-irradiated mice, while no effect of radiation was observed in KO mice. CONCLUSIONS: These studies show that apoE expression influences the behavioral toxicity of HZE particle radiation and suggest that apoE plays a role in the repair/recovery from radiation injury of the CNS. ApoE deficiency may exacerbate the previously reported effects of HZE particle radiation in accelerating the brain aging process.

Full Text

Duke Authors

Cited Authors

  • Higuchi, Y; Nelson, GA; Vazquez, M; Laskowitz, DT; Slater, JM; Pearlstein, RD

Published Date

  • December 2002

Published In

Volume / Issue

  • 43 Suppl /

Start / End Page

  • S219 - S224

PubMed ID

  • 12793762

Pubmed Central ID

  • 12793762

International Standard Serial Number (ISSN)

  • 0449-3060

Digital Object Identifier (DOI)

  • 10.1269/jrr.43.s219

Language

  • eng

Conference Location

  • England