Authors
Liu J. Wang X. Shigenaga MK. Yeo HC. Mori A. Ames BN.
Institution
Molecular and Cell Biology, Division of Biochemistry and Molecular Biology,
University of California, Berkeley 94720, USA.
Title
Immobilization stress causes oxidative
damage to lipid, protein, and DNA in the brain of rats [see comments].
Comments
Comment in: FASEB J 1997 Apr;11(5):374-5
Source
FASEB Journal. 10(13):1532-8, 1996 Nov.
Abstract
Immobilization stress of male
Sprague-Dawley rats induces oxidative damage to lipid, protein, and DNA in
the brain. Significant increases in lipid peroxidation were found in the
cerebral cortex, cerebellum, hippocampus, and midbrain compared to the
unstressed controls. Significant increases in levels of
protein oxidation were also found in the cortex, hypothalamus, striatum, and
medulla oblongata. Oxidative nuclear DNA damage increased after
stress in all brain regions, although only the cerebral
cortex showed a significant increase. Depletion of glutathione showed some
stimulation to oxidative damage in the unstressed control
and stressed animals. Further studies of the mitochondrial
and cytosol fractions of cerebral cortex demonstrated that mitochondria
showed a significantly greater increase in lipid peroxidation and protein
oxidation than cytosol. Data from plasma and liver showed oxidative damage
similar to that of the brain. These findings provide evidence to support the
idea that stress produces oxidants, and that the oxidative
damage in stress could contribute to the degenerative
diseases of aging, including brain dysfunction.