The antioxidative effect of quercetin, quercetin 3-O-beta-D-glucopyranoside (Q3G), quercetin 4'-O-beta-D-glucopyranoside (Q4'G) and quercetin 7-O-beta-D-glucopyranoside (Q7G) was examined in solution and liposomal phospholipid suspension. First, their peroxyl radical-scavenging activities were investigated by measuring the inhibition of hydroperoxidation of methyl linoleate initiated by a radical initiator, 2,2'-azobis(2,4-dimethylvaleronitrile) (AMVN). Quercetin exhibited the highest peroxyl radical-scavenging activity judging from the rate of hydroperoxidation during the induction period (Rinh) and the length of induction period (tinh). Although Q7G showed an induction period, its Rinh was higher and its tinh was lower than that of quercetin. Neither Q3G nor Q4'G gave a clear induction period in the curve of hydroperoxide formation. The rate of hydroperoxidation in the presence of Q3G was higher than Rinh of quercetin and the oxidative loss of Q3G was much slower than quercetin or Q7G when exposed to AMVN in solution. Q4'G exerted little inhibition compared to Q3G or Q7G. Next, the antioxidative activity of quercetin and its monoglucosides in phospholipid bilayers was examined by measuring the inhibition of lipid peroxidation in large unilamellar vesicles composed of egg yolk phosphatidylcholine (PC) and a water-soluble radical initiator. They retarded the accumulation of PC-hydroperoxides and the induction period increased in the order of Q4'G < Q3G approximately Q7G < quercetin. It is therefore concluded that quercetin acts as an antioxidant more efficiently than its monoglucosides when phospholipid bilayers are exposed to aqueous oxygen radicals.

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In order to evaluate the positional specificity for a glucoside group in the hydrolysis of flavonoid glucosides in the rat small intestine, beta-glucosidase activity was measured with the quercetin monoglucosides, quercetin-3-O-beta-D-glucopyranoside (Q3G), quercetin-4'-O-beta-D-glucopyranoside (Q4'G) and quercetin-7-O-beta-D-glucopyranoside (Q7G), as well as with quercetin-3-O-rutinoside (rutin) and p-nitrophenyl-beta-D-glucopyranoside (NPG) by using the HPLC technique. Enzymes were prepared from rat small intestinal mucosa of the duodenum, jejunum and ileum, among which the enzyme activity of the jejunum was highest for all the glycosides tested. Q4'G was the richest substrate for a beta-glucosidase solution among these glycosides, while rutin and NPG were both poor substrates. This suggests that dietary flavonoid glucosides are primarily hydrolyzed and liberated aglycones in the jejunum.

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Information processing deficits in major depressive disorder have been infrequently examined electrophysiologically. Its preattentive and sensory information processing was examined using mismatch field (MMNm) and P1m components, respectively, by magnetoencephalography. Fourteen major depressive disorder patients and 19 healthy volunteers participated in the study. MMNm was elicited in response to duration and frequency changes of pure-tone stimuli and in response to a vowel across-category change. The magnetic global field power (mGFP) of MMNm was significantly smaller in the major depressive disorder patients than in the healthy volunteers, although that of P1m did not differ between the two groups. Information processing at the preattentive level is impaired functionally in major depressive disorder, and this dysfunction is not due to the dysfunction at the lower level of information processing.