No abstract

Although the antioxidant properties of green, oolong, and black teas have been well studied, antioxidant activity has not been examined in roasted tea. Therefore, in the current studies, we investigated the antioxidant activity of roasted tea in comparison with those of green, oolong, and black teas. Using water extracts of the various teas, we examined the total phenolic content as well as the antioxidant activities, including the reducing power, the 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity, and the inhibition of hemolysis caused by 2,2'-azo-bis(2-amidinopropane) dihydrochloride (AAPH)-induced lipid oxidation in erythrocyte membranes. The roasted tea contained lower levels of total phenolics than green, oolong, or black tea (green tea > oolong tea > black tea > roasted tea). The relative reducing power and DPPH scavenging activity decreased in the following order: green tea > roasted tea > oolong tea > black tea. Also, green tea was more effective against AAPH-induced erythrocyte hemolysis than other teas (green tea>roasted tea = oolong tea = black tea). These results suggest that roasted tea is beneficial to health, in humans, because of its high antioxidant activity.

No abstract

Ouabain (5 x 10(-8)-5 x 10(-4) M) was confirmed to cause a dose-dependent increase in [3H]acetylcholine ([3H]ACh) release, cytosolic free Ca2+ concentration ([Ca2+]i), and 22Na+ uptake in cerebrocortical synaptosomes of rats in the presence of extracellular Ca2+. Ouabain also caused a dose-dependent decrease in membrane potential. In a low-Na+ (10 mM) medium, ouabain failed to increase [3H]ACh release and [Ca2+]i. Tetrodotoxin (10(-6) M) had no effect on the ouabain-induced increase in both [3H]ACh release and [Ca2+]i but abolished the increase in 22Na+ uptake and partially inhibited the depolarizing effect. Verapamil (10(-6)-5 x 10(-4) M) inhibited the ouabain-induced increase in both [3H]ACh release and [Ca2+]i in a dose-dependent manner. Removal of extracellular Ca2+ abolished the effect of ouabain on [Ca2+]i but not on [3H]ACh release and 22Na+ uptake, regardless of the presence or absence of EGTA. In the absence of extracellular Ca2+, 10 mM Mg2+ blocked ouabain-induced [3H]ACh release, which was resistant to verapamil. These results suggest that ouabain can increase ACh release from synaptosomes without the preceding increases in intracellular Ca2+ and/or Na+ content. It seems likely that the removal of extracellular Ca2+ unmasks mechanisms of ouabain action different from those operating in the presence of Ca2+.