title: Green tea consumption and serum malondialdehyde-modified LDL concentrations in healthy subjects.
abstract: OBJECTIVE
  Green tea was shown to inhibit LDL oxidation, platelet aggregation, and matrix metalloproteinases (MMPs) activities in vitro. We tried to elucidate whether or not green tea consumption may have these effects in vivo, which may be protective against atherosclerotic disease.
  
  
  METHODS
  We measured serum malondialdehyde-modified LDL (MDA-LDL) concentrations and urine 8-epi-prostaglandin (PG) F(2alpha) in 22 healthy male nonsmokers. They drank 7 cups/day of water for 2 weeks and drank 7 cups/day of green tea for the next 2 weeks. Regarding platelet aggregation, plasma thromboxane B(2) (TXB(2)) and 6-keto-PGF(1alpha) concentrations and ex vivo platelet aggregation were evaluated. Plasma MMP-2 and -9 concentrations were also measured.
  
  
  RESULTS
  Of the 22 subjects, 20 had been in the habit of drinking green tea before the study. Plasma catechins concentrations significantly decreased at the end of the water period and then increased at the end of the green tea period. Although no change in plasma LDL-cholesterol concentrations (110 +/- 33 vs. 113 +/- 28 mg/dL, p = NS) was found, MDA-LDL concentrations (84 +/- 45 vs. 76 +/- 40 IU/L, p < 0.05) and the ratio of MDA-LDL/LDL-cholesterol (0.74 +/- 0.21 vs. 0.65 +/- 0.20, p < 0.02) significantly decreased at the end of the green tea period. However, no significant changes were observed in urine 8-epi-PGF(2alpha) concentrations, in platelet aggregation, nor in plasma TXB(2), 6-keto-PGF(1alpha) or MMP concentrations.
  
  
  CONCLUSIONS
  Daily consumption of green tea decreased serum MDA-LDL concentrations, but it had no significant effects on platelet aggregation, platelet TX production or plasma MMPs concentrations. Our results suggest that green tea consumption may inhibit LDL oxidation in vivo.
authors.affiliation: First Department of Internal Medicine, National Defense Medical College, Tokorozawa, Saitama 359-8513, Japan. rhirano@yahoo.co.jp
authors.forename: Reiko
authors.initials: R
authors.lastname: Hirano-Ohmori
authors.forename: Rie
authors.initials: R
authors.lastname: Takahashi
authors.forename: Yukihiko
authors.initials: Y
authors.lastname: Momiyama
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Taniguchi
authors.forename: Atsushi
authors.initials: A
authors.lastname: Yonemura
authors.forename: Seiichi
authors.initials: S
authors.lastname: Tamai
authors.forename: Keizo
authors.initials: K
authors.lastname: Umegaki
authors.forename: Haruo
authors.initials: H
authors.lastname: Nakamura
authors.forename: Kazuo
authors.initials: K
authors.lastname: Kondo
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Ohsuzu
mesh_terms: D000328:Adult; D000975:Antioxidants / Q000494:pharmacology; D002392:Catechin / Q000097:blood / Q000378:metabolism* / Q000494:pharmacology*; D018592:Cross-Over Studies; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000097:blood / Q000378:metabolism*; D045726:Metalloproteases / Q000097:blood / Q000187:drug effects; D010084:Oxidation-Reduction; D010974:Platelet Aggregation / Q000187:drug effects; D013662:Tea
chemical_list: D000975:Antioxidants; D008077:Lipoproteins, LDL; D013662:Tea; C075750:8-epi-prostaglandin F2alpha; D008315:Malondialdehyde; D002392:Catechin; D015237:Dinoprost; D045726:Metalloproteases