In order to define whether active oxygen species actually induce oxidative damage to the nervous system, and how antioxidative defense systems are changed by oxidative stress, morphological and functional changes in the nervous system and antioxidant status were investigated. When rats were exposed to 100% oxygen in a chamber, many morphological changes, e.g. swollen astrocytes around vessels, deformed nuclei in nerve cells, pigmentation, swollen mitochondria, and abnormal accumulation of synaptic vesicles in swollen nerve terminals, were observed by electron microscopy. When synaptosomes isolated from oxygen-exposed rats were stimulated by KCI, acetylcholine release from the terminal was decreased more significantly than in synaptosomes from unexposed rats ( P < 0.01). Synaptic plasma membrane fluidity decreased in response to oxygen exposure, and plasma membrane permeability to sucrose was increased significantly ( P < 0.05). The cholesterol/phospholipid ratio of the plasma membranes was increased by oxidative stress and the content of unsaturated fatty acids, especially arachidonic acid and docosahexaenoic acid, decreased. The levels of thiobarbituric-acid-reactive substances in the plasma membranes of oxygen-exposed rats were significantly higher than in unexposed rats ( P < 0.01).These results suggest that free radicals derived from oxygen may attack nerve terminals and peroxidize the plasma membrane. It was found that in response to the oxidative stress, the status of the defense system in synapse, i.e. the concentration of vitamin E, activities of superoxide dismutase and glutathione peroxidase changed, and that many of the changes observed were reduced remarkably by the intraperitoneal administration of vitamin E prior to stress. Data support the idea that vitamin E contributes to the protection against nerve dysfunction caused by oxidative stress.
The antioxidant activity of 10 Japanese and Chinese crude drugs (Kampo drugs) was determined in vitro. Extract of Magnolia cortex, which had the highest antioxidant activity, contained phenolic compounds magnolol and honokiol. However, inhibitory effects of these compounds on lipid oxidation were weaker than that of α-tocopherol as measured by thiobarbituric acid assay. The structure-activity relationship of phenolic compounds showed that antioxidant activities were in the order 4-allyl-2,6-dimethoxyphenol ≥ p,p′-biphenol > eugenol > 2-allyl-6-methylphenol > honokiol > magnolol > caffeic acid > p-ethylphenol > guaiacol. As expected, these results showed that an electron donor and/or bulky groups at the ortho-or paraposition of the phenol were required for inhibition of lipid oxidation. Electron spin resonance spin trapping experiments showed that phenol compounds with an allyl substituent on their aromatic rings directly scavenged superoxide (O 2 − ), and that only eugenol trapped hydroxyl radicals. These findings suggest that phenolic compounds that contain allyl groups may be effective antioxidants because of the scavenging ability of O 2 − or hydroxyl radical, whereas other phenols, without an allyl moiety such as α-tocopherol, may play a role in the termination of free radical chain reactions. JAOCS 74, 557-562 (1997).
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