title: Effects of theanine on alcohol metabolism and hepatic toxicity.
abstract: We previously showed that theanine, is a major amino acid in green tea, enhanced doxorubicin (DOX) induced antitumor activity. Besides, theanine induced the elevation of glutathione (GSH) level attributable to the increase of glutamate in the liver of mice, namely theanine would reduce the adverse reaction of DOX. Consequently, theanine was thought to be effective against the tissue changes with GSH level reduction. On the other hand, it is suggested excessive uptake of alcohol causes a production of free radicals, a decrease of GSH level, and an increase in the amount of lipid peroxide (LPO) in liver, and shifting to an alcoholic liver injury. Then, aiming at the prevention and medical treatment of a hepatic toxicity by the food components with little toxicity, we have studied the effect of theanine (i.p.) on ethanol metabolism and hepatic toxicity using ethanol (p.o.) single-administered mice. On the 1st hour after ethanol administration, the ethanol concentrations in blood of the theanine combined groups decreased compared with the ethanol-alone group. The alcohol dehydrogenase and aldehyde dehydrogenase activities in the liver increased by combined theanine. Since the elevation of cytochrome P450 (CYP) 2E1 activity was controlled in the theanine-combined groups, it was considered that these disorders attributable to CYP2E1 in ethanol long-term uptake might be avoidable by theanine. Although LPO increased in 3 h after by single-administration of ethanol, the increase was controlled by theanine-administration and was improved until the normal level. In conclusion, it was indicated that theanine was effective against alcoholic liver injury.
authors.affiliation: School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka, Japan. sadzuka@u-shizuoka-ken.ac.jp
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Sadzuka
authors.forename: Chieko
authors.initials: C
authors.lastname: Inoue
authors.forename: Saho
authors.initials: S
authors.lastname: Hirooka
authors.forename: Tomomi
authors.initials: T
authors.lastname: Sugiyama
authors.forename: Keizo
authors.initials: K
authors.lastname: Umegaki
authors.forename: Takashi
authors.initials: T
authors.lastname: Sonobe
mesh_terms: D000444:Aldehyde Dehydrogenase / Q000378:metabolism; D000818:Animals; D002492:Central Nervous System Depressants / Q000378:metabolism* / Q000493:pharmacokinetics / Q000633:toxicity*; D056486:Chemical and Drug Induced Liver Injury / Q000201:enzymology / Q000473:pathology / Q000517:prevention & control*; D019392:Cytochrome P-450 CYP2E1 / Q000378:metabolism; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D000431:Ethanol / Q000378:metabolism* / Q000493:pharmacokinetics / Q000633:toxicity*; D005971:Glutamates / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D007274:Injections, Intraperitoneal; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000201:enzymology / Q000473:pathology; D051379:Mice; D014018:Tissue Distribution
chemical_list: D002492:Central Nervous System Depressants; D005971:Glutamates; D000431:Ethanol; C026166:theanine; D003577:Cytochrome P-450 Enzyme System; D019392:Cytochrome P-450 CYP2E1; D000444:Aldehyde Dehydrogenase; D005982:Glutathione Transferase; D005978:Glutathione