green and black teas and atherosclerosis

From: Doug Skrecky (oberon@vcn.bc.ca)
Date: Fri May 29 1998 - 00:40:26 MDT


Authors
  Tijburg LB. Wiseman SA. Meijer GW. Weststrate JA.
Institution
  Unilever Research Laboratorium, Vlaardingen, The Netherlands.
  Lilian.Tijburg:Unilever.com
Title
  Effects of green tea, black tea and dietary lipophilic antioxidants on LDL
  oxidizability and atherosclerosis in hypercholesterolaemic
  rabbits.
Source
  Atherosclerosis. 135(1):37-47, 1997 Nov.
Abstract
  The hypothesis that tea or dietary lipid-soluble antioxidants reduce
  atherogenesis by lowering the oxidizability of low-density lipoprotein (LDL)
  was investigated. Five groups of 20 female New Zealand white rabbits were fed
  a restricted amount of a high-fat (30 en%) semipurified diet supplemented
  with cholesterol (0.15%, w/w) for 21 weeks. The vitamin E content of the
  control diet was 40 mg/kg diet. The animals received either green tea or
  black tea in their drinking water or vitamin E (200 mg/kg diet) or
  beta-carotene (20 mg/kg). The serum cholesterol concentrations (in the order
  of 18-23 mmol/l) were not significantly different between the groups. Vitamin
  E was substantially increased as compared to controls in vitamin E
  supplemented animals (3-fold within 8 weeks in plasma and LDL; P < 0.01) and
  weakly (1.2-fold) by green and black tea (P < 0.05). Green tea consumption
  tended to reduce aortic lesion formation by 31% (24 +/- 3.2% versus 35 +/-
  5.7% for control animals P = 0.11), while black tea, vitamin E and
  beta-carotene had no effect. This was in contrast to the resistance of
  isolated LDL to oxidation induced at high copper concentration. Green and
  black tea induced a 13% and 15% (P < 0.05) prolongation of the lag phase,
  respectively, with a correspondingly lower oxidation rate, while vitamin E
  increased the lag phase by 63% (P < 0.01) with a concomitant diminution of
  the oxidation rate and beta-carotene had no effect. Regression analysis
  showed that there was no relationship between the extent of
  atherosclerosis and LDL oxidizability or plasma
  malondialdehyde as marker of in vivo lipid peroxidation. The results of the
  present study raise the question whether LDL oxidizability (at least when
  tested at high induction rate ex vivo) is a primary causal mechanism in
  atherosclerosis in the cholesterol-fed rabbit. The
  suitability of the cholesterol-fed rabbit with extreme hypercholesterolaemia
  as a model to study antiatherosclerotic properties of dietary antioxidants,
  such as the tested polyphenols, is discussed.



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