Address for correspondence: Shiro Urano, Division of Biological Chemistry, Shibaura Institute of Technology, 3-9-14 Shibaura, Minato-ku, Tokyo 108-8548, Japan. Voice: +81-3-5476-2429, fax: +81-3-5476-3162.
urano{at}sic.shibaura-it.ac.jp
Ann. N.Y. Acad. Sci. 959: 275-284 (2002).
In order to verify whether brain damage caused by chronic oxidative
stress induces the impairment of cognitive function, the ability
of learning and memory was assessed using the water maze and
the eight-arm radial maze tasks. Young rats showed significantly
greater learning ability before the stress than the old and
vitamin E-deficient rats. At five days after subjection to oxidative
stress, the memory function of the young declined toward the
level of that in the aged rats maintained under normal condition.
This phenomenon is supported by the findings that the delayed-type
apoptosis appeared in the CA1 region of the hippocampus of the
young at five to seven days after the stress. Vitamin E supplementation
to the young accelerated significantly their learning functions
before the stress and prevented the deficit of memory caused
by the stress. When rats were subjected to stress, thiobarbituric
acid-reactive substance (TBARS), lipid hydroperoxides, and protein
carbonyls were significantly increased in synaptic plasma membranes.
It was found that
-potential of the synaptic membrane surface
was remarkably decreased. These phenomena were also observed
in the aged and vitamin E-deficient rats maintained under normal
condition. These results suggest that oxidative damage to the
rat synapse in the cerebral cortex and hippocampus during aging
may contribute to the deficit of cognitive functions.
