X-Message-Number: 24711
Date: Fri, 24 Sep 2004 20:14:41 -0700 (PDT)
From: Doug Skrecky <>
Subject: Ardisia compressa tea

(Looks like good stuff, but where can one buy it?)

Food Chem Toxicol. 2004 Mar;42(3):509-16.
Inhibition of liver carcinogenesis in Wistar rats by consumption of an
aqueous extract from leaves of Ardisia compressa.
  This study evaluates the chemopreventive effect of an aqueous extract of
dried leaves of Ardisia compressa against liver cancer. A rat liver assay
that mimics progressive forms of human disease was used as a
carcinogenesis model. Forty-five male Wistar rats (180-200 g body weight)
were injected intraperitoneally on day 1 with a single dose (100 mg/kg) of
diethylnitrosamine (DEN), and also received via gavage 20 mg/kg
acetylaminofluorene (2-AAF), on days 7, 8 and 9. The rats were randomly
divided into four groups (n=15). Control groups (Group 1 and Group 2) had
free access to water. Group 3 received 0.5% (w/v) of A. compressa tea for
10 days before treatment and during the study as the sole source of fluid
until the rats were killed. A fourth group of 15 rats received no
carcinogen or promoter but did receive 0.5%, (w/v) of A. compressa tea.
All animals had 70% partial hepatectomy at day 10. The incidences of
hepatocellular foci, nodules and carcinoma were significantly smaller in
Group 3 than in Group 2 (P<0.01). A. compressa tea consumption alone
(Group 4) did not induce the development of foci, nodules or carcinomas
(P<0.01). The striking observation of this study was that consumption of
A. compressa tea resulted in complete inhibition of the
chemically-induced hepatocarcinogenesis in Wistar rats.

J Agric Food Chem. 2002 Dec 18;50(26):7714-9.
Topoisomerase I and II enzyme inhibitory aqueous extract of Ardisia
compressa and ardisin protect against benomyl oxidation of hepatocytes.
  Tea preparations of Ardisia compressa (AC) have been used in folk
medicine against liver disorders. The objective of this study was to
evaluate the in vitro topoisomerase I and II enzyme inhibition and the
antioxidant effect of an aqueous extract from dry leaves of AC and a pure
component (ardisin) purified from AC on benomyl (Be)-induced cytotoxicity
in primary culture rat hepatocytes. Lipid peroxidation (malondialdehyde),
antioxidant enzyme activities of glutathione reductase, glutathione
peroxidase, and superoxide dismutase, and glutathione levels were
studied. Topoisomerase I and II enzyme inhibition was used to guide
purification of ardisin, which was purified using TLC, MPLC, and
preparative and analytical HPLC methods. Benomyl increased
malondialdehyde (58% change in comparison to the control) and glutathione
peroxidase (10%), producing a significant consumption of endogenous
antioxidant glutathione (65%, P < 0.05). A 94% hepatocyte protection was
observed when cells were first exposed to ardisin (0.27 microg/mL),
followed by Be (35 microg/mL). Cell protection by the tea extract of AC
(AE) was greater than that by (-)-epigallocatechin 3-gallate (EGCG).
Ardisin showed a clear inhibition of topoisomerases I and II catalytic
activity in Saccharomyces cerevisiae mutant cells JN 394, JN394t(-)(1),
and JN394t-(2)(-)(5). The potency of ardisin was superior to that of AE
and EGCG as an antioxidant, protecting rat hepatocytes when exposed to
Be. On the basis of the effective concentrations of equivalents to
[+]catechin found in the present study, it can be estimated that, in
order to gain antioxidative protection, a person would need to ingest
approximately 1 L of AC tea per day, with a total content of 10.8 g of
plant material.

Toxicology. 2002 Sep 30;179(1-2):151-62
Leaf extract from Ardisia compressa protects against
1-nitropyrene-induced cytotoxicity and its antioxidant defense disruption
in cultured rat hepatocytes.
  Herbal tea preparations of Ardisia compressa (AC) have been used in folk
medicine against liver disorders. The objective of this study was to
evaluate the in vitro protective effect of an aqueous extract of dry
leaves of AC on 1-nitropyrene (1-NP) induced cytotoxicity on rat
hepatocytes. Lipid peroxidation (malondialdehyde), antioxidant enzyme
activities (glutathione reductase, glutathione peroxidase, superoxide
dismutase) and glutathione levels were studied. After 2 h of incubation,
0.25 microg/ml of 1-NP had an approximately 50% cytotoxic effect on
hepatocytes. This environmental toxicant also increased malondialdehyde
(77%), and glutathione peroxidase (46%), producing a significant
consumption of endogenous antioxidant glutathione. (-)Epigallocatechin
3-gallato (EGCG) and AC decreased the viability of hepatocytes after 2 h
of incubation at concentrations above 3 microg/ml and 2.52 microg,
equivalents of (+)catechin/ml, respectively. A 100% hepatocyte protection
was observed when cells were first exposed to AC (2.52 microg,
equivalents of (+)catechin/ml), and then followed by 1-NP (0.25
microg/ml). Cells incubated with AC, either simultaneously or before
treatment with 1-NP, were protected 75 and 84%, respectively. Cell
protection of AC was superior to EGCG. Addition of AC to 1-NP (1:10)
modulated superoxide dismutase and glutathione reductase activities
(P<0.005), as well as the cellular level of GSH. The results indicate
that AC has an antioxidant protective effect on rat hepatocytes when
exposed to 1-NP.

J Agric Food Chem. 2004 Jun 2;52(11):3583-9
Polyphenolic compounds, antioxidant capacity, and quinone reductase
activity of an aqueous extract of Ardisia compressa in comparison to mate
(Ilex paraguariensis) and green (Camellia sinensis) teas.
  Aqueous extracts of the leaves of Ardisia compressa (AC) have been used
in folk medicine to treat various liver disorders including liver cancer.
The objective of this study was to partially characterize and determine
the total polyphenol content, antioxidant capacity, and quinone reductase
activity of A. compressa tea in comparison to mate (Ilex paraguariensis,
MT) and green (Camellia sinensis,GT) teas. Total polyphenol content,
antioxidant capacity, and phase II enzyme induction capacity were
measured by the modified Folin-Ciocalteu, ORAC, and quinone reductase
(QR) assays, respectively. The major polyphenols in AC were not catechins.
HPLC retention times and standard spikes of AC indicated the presence of
gallic acid, epicatechin gallate, ardisin and kaempferol. Using catechin
as standard, the total polyphenol value of AC (36.8 +/- 1.1 mg/mg DL) was
significantly lower than GT (137.2 +/- 5.8 mg equivalent of
(+)-catechin/mg dried leaves, DL) and MT (82.1 +/- 3.8 mg/mg DL) (P <
0.001). Antioxidant capacity (AC, 333; GT, 1346; MT, 1239 mmol Trolox
equivalents/g DL) correlated with total polyphenol values (r(2) = 0.86, P
< 0.01). AC (4.5-12.5 microg/mL) induced QR enzyme, in
Hepa1c1c7 cells, up to 15%. MT and GT showed no induction at the
concentrations tested (0.5-10.5 and 0.5-12.5 mg/mL, respectively). These
results suggest that AC has a different mechanism of protection against
cytotoxicity that is not related to its antioxidant capacity. Further
studies are needed to determine such mechanisms and to explore its
potential as a chemopreventive or therapeutic agent.

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