green and black teas and atherosclerosis
Doug Skrecky (oberon@vcn.bc.ca)
Thu, 28 May 1998 23:40:26 -0700 (PDT)
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.