Influence of oxidative stress on fusion of pre-synaptic plasma membranes of the rat brain with phosphatidyl choline liposomes, and protective effect of vitamin E.

Influence of oxidative stress on fusion of pre-synaptic plasma membranes with phosphatidylcholine (PC) liposomes as a model of synaptic vesicle was investigated. The inhibitory effect of vitamin E on the decline in the fusion caused by oxidative stress was also assessed. Rats subjected to hyperoxia as oxidative stress showed significant increases in the levels of lipid hydroperoxides and protein carbonyl moieties in pre-synaptic plasma membranes in the brain.

Oxidative damage of rat cerebral cortex and hippocampus, and changes in antioxidative defense systems caused by hyperoxia.

In order to elucidate the oxidative damage in rat brain caused by oxidative stress, regional changes in the levels of lipid peroxidation products and antioxidative defense systems in cerebral cortex and hippocampus, and in their synapses, which modulate learning and memory functions in the brain, were studied. When rats were subjected to hyperoxia as an oxidative stress, thiobarbituric acid reactive substance (TBARS) in the regions studied increased more than in normal rats by approximately 35%. The values in oxygen-unexposed vitamin E-deficient rats were also higher than in normal rats.

Cognitive impairment of rats caused by oxidative stress and aging, and its prevention by vitamin E.

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.