HERBAL MEDICINAL
Camellia sinensis (L.) Kuntze var. green tea
J. C. Lettsom, The Natural History of The Tea Tree, 2nd Ed.,p.i (1799) [J. Miller]
Camellia
sinensis (L.) Kuntze var. green tea
BOTANICAL
DESCRIPTION (Ross, I. A. 2005)
Camellia sinensis is an evergreen tree or shrub of the THEACEAE family that grows
to 10–15 m high in the wild, and 0.6–1.5 m under cultivation. The leaves are
shortstalked, light green, coriaceous, alternate, elliptic-obovate or
lanceolate, with serrate margin, glabrous, or sometimes pubescent beneath, varying
in length from 5 to 30 cm, and about 4 cm wide. Young leaves are pubescent.
Mature leaves are bright green in color, leathery, and smooth.
Flowers are white, fragrant, 2.5–4 cm in diameter, solitary or in clusters of
two to four. They have numerous stamens with yellow anthers and produces brownish-red,
one- to four-lobed capsules. Each lobe contains one to three spherical or
flattened brown seeds. There are numerous varieties and races of tea.
There are three main groups of the cultivated forms: China, Assam,
and hybrid tea, differing in form. Camellia sinensis assamica, the source
of much of the commercial tea crop of Ceylon is a tree that, unpruned, may
attain a height of 15 m and has proportionally longer, thinner leaves than
typical species.
ORIGIN AND DISTRIBUTION (Ross, I. A. 2005)
The cultivation and enjoyment of tea are recorded in Chinese
literature of 2700 BC and in Japan about 1100. Through the Arabs, tea reached Europe
about 1550. Native to Assam, Burma, and the Chinese province of Yunnan, it is
highly regarded in southern Asia and planted in India, southern Russia, East
Africa, Java, Ceylon, Sumatra, Argentina, and Turkey.
China, India, Indonesia, and Japan produced about a half of the
total world production.
THE
MAIN TYPES OF TEA INCLUDE (Dole
Food Company, Inc. 2002) :
Types Of Tea Include :
Green
tea—A favorite
in Asia, green tea is so named because the leaves are dried and fragmented soon
after picking. Tea made from these leaves is mild and fresher in taste than
other types of tea. Because of this, green tea usually is not served with milk
or sugar. Types of green tea include gunpowder, Tencha, and Gyokuro, a Japanese
tea also known as pearl dew tea.
Black
tea—Actually a
dark reddish brown tea when it is brewed, the strongly flavored black tea is
popular in Western nations. It is the most processed and strongest flavored
tea. After the leaves are picked, they are allowed to ferment in the open sun
before being dried. The size of the tea leaves determines the grading of black tea.
Common black tea varieties include Ceylon, Assam, and Darjeeling, considered by
many to be the finest black tea.
Oolong
teas—Oolong tea has characteristics of both black and green teas.
Its leaves are fermented for about half the time of black tea. Oolong tea
originated in the Fukien province of China, where much of the world’s
production of oolong tea takes place. Formosan tea, named for the former name of
Taiwan, is considered by many to be the finest oolong tea.
Blended
teas—Often referred to as English teas, these are black teas that
have been blended
with spices and flavorings to enhance
tea flavor and aroma. Thousands of
blended teas are available worldwide. Popular
blended teas include English breakfast and
Earl Grey.
Herbal
teas—Not made
from tea leaves, herbal tea is a tea-like drink made by steeping herbs,
flowers, and spices in heated water. Herbal tea has been made throughout history,
often for medicinal purposes or simply to make water taste better. Popular herbal
teas are made from chamomile, rose hips, and mint, to name just a few. In France,
herbal teas are referred to as “tisanes.” Herbal teas typically contain no
caffeine.
Instant
tea—Popular in
the United States since the 1950s, instant tea is tea that has been dehydrated
and granulated so that it dissolves rapidly in water. Often, it also contains
sugar and other flavorings. Store tea away from heat in a sealed container. Tea
keeps for about 6 months. After that, it loses its flavor and should be
discarded.
TRADITIONAL MEDICINAL USES (Ross, I. A. 2005)
India. Decoctions of the
dried and fresh buds and leaves are taken orally for headache and feverCS145. Powder or
decoction of the dried leaf is applied to teeth to prevent tooth decayCS146. Fresh leaf juice
is taken orally for abortionCS155, and as a contraceptive and
hemostaticCS147.
Mexico. Hot water extract
of the leaf is taken orally by nursing mothers to increase milk productionCS148.
Turkey. Leaves are taken
orally to treat diarrheaCS149.
China. Hot water extract
of the dried leaf is taken orally as a sedative, an antihypertensive, and
anti-inflammatoryCS108.
Guatemala. Hot water extract
of the dried leaf is used as eyewash for conjunctivitisCS154.
Kenya. Water extract of
the dried leaf is applied ophthalmically to treat corneal opacitiesCS150. The infusion is
used for chalzion and conjunctivitisCS151. Thailand. Hot water
extract of the dried leaf is taken orally as a cardiotonic and neurotonicCS152. Hot water extract
of the dried seed is taken orally as an antifungalCS153.
CHEMICAL CONSTITUENTS (Ross, I. A. 2005)
(ppm
unless otherwise indicated)
Acetaldehyde,
phenyl: Sh 1.52–1.78%CS100
Acetaldehyde:
LfCS073
Acetamide,
N-ethyl: LfCS027
Acetic
acid: LfCS086
Acetoin:
LfCS068
Acetone:
LfCS091
Acetophenone,
2-4-dimethyl: LfCS027
Acetophenone,
3-4-dimethoxy: LfCS027
Acetophenone,
para-ethyl: LfCS027
Acetophenone:
Headspace volatileCS044
Actinidiolide,
dihydro: Lf EOCS132
Afzelechin,
epi, (–): Lf 350CS084
Afzelechin,
epi, 3-O-gallate (–): Lf 37CS005
Afzelechin,
epi, 3-O-gallate (4-b-6)-epi,
gallocatechin-3-O-gallate:
Lf 5.6CS008
Allantoic
acid: PlCS033
Allantoin:
PlCS033
Aluminium
inorganic: LfCS028
Amyrin,
: Sd oilCS095
Amyrin,
: Sd oil 76CS095
Aniline,
N-ethyl: LfCS027
Aniline,
N-methyl: LfCS027
Aniline:
LfCS027
Apigenin:
LfCS108
Apigenin-6-8-di-C--D-arabinopyranosyl:
Lf 20CS156
Apigenin-6-8-di-C-glucoside:
ShCS096
Arbutin:
Lf 0.2CS078
Aromadenrin:
ShCS094
Ascorbic
acid: ShCS038, Lf 0.257%CS048
Assamicain
A: Lf 58.2CS007
Assamicain
B: Lf 76.6CS007
Assamicain
C: Lf 33.6CS007
Assamsaponin
A: Sd 0.01%CS021
Assamsaponin
B: Sd 28.3CS021
Assamsaponin
C: Sd 36.5CS021
Assamsaponin
D: Sd 26.1CS021
Assamsaponin
E: Sd 11.1CS021
Assamsaponin
F: Sd 14.1CS021
Assamsaponin
G: Sd 79.1CS021
Assamsaponin
H: Sd 13.4CS021
Assamsaponin
I: Sd 98.5CS021
Astragalin:
LfCS139
Avicularin:
LfCS058
Barrigenol,
A-1: PlCS118
Barringtogenol
C, 3-O--D-galactopyranosyl(1-2) -D-xylopyranosyl (1-2)-l-arabinopyranosyl(1-3)-Dglucuronopyranosyl-21-O-cinnamoyl-16-22-di-O-acetyl:
LfCS013
Benzene,
1-2-3-trimethoxy: LfCS077
Benzene,
1-2-3-trimethoxy-5-ethyl: LfCS077
Benzene,
1-2-3-trimethoxy-5-methyl: LfCS077
Benzene,
1-2-4-trihydroxy: LfCS003
Benzene,
1-2-5-trihydroxy: LfCS003
Benzene,
1-2-dimethoxy: LfCS077
Benzene,
1-2-dimethoxy-4-ethyl: LfCS077
Benzene,
1-2-dimethoxy-4-methyl: LfCS077
Benzene,
1-3-diacetyl: LfCS027
Benzene,
1-4-diacetyl: LfCS027
Benzoic
acid: Headspace volatileCS044
Benzothiazole,
2-methyl: LfCS036
Benzothiazole:
LfCS036
Benzoxazole:
LfCS036
Benzyl
alcohol: Lf EO 1.01–1.6%CS136,
Headspace
volatileCS044, LfCS091,
Sh
0.09–0.14%CS100
Benzyl
butyrate: LfCS002
Benzyl
ethyl ketone: LfCS002
Benzylaldehyde,
2-methyl: LfCS002
Benzylaldehyde,
4-methoxy: LfCS002
Benzylaldehyde:
Headspace volatileCS044,
LfCS077, Sh 0.21–0.23%CS100
Benzylamine:
N-N-dimethyl: LfCS027
Bicyclo(4.3.0)non-8-en-7-one,
1-5-5-9-
tetramethyl:
LfCS002
Brassicasterol:
Sd oilCS134
Brassinolide,
28-homo, 6-keto: LfCS135
Brassinolide,
28-nor, 6-keto: LfCS135
Brassinolide,
28-nor: LfCS135
Brassinolide,
6-keto: LfCS135
Brassinolide:
Lf 0.0046 ppbCS089
Brassinone,
24(S)-ethyl: Lf 30 ng/65 kgCS110
Brassinone,
24-ethyl: LfCS089
Brassinone:
Lf 130 ng/65 kgCS110
Butan-2-ol:
LfCS068
Butyrate,
ethyl-3-hydroxy: LfCS068
Butyroin:
LfCS068
Butyrospermol:
Sd oilCS095
Caffeine:
Lf 0.381–9.9%CS114,CS049, ShCS038, Pl,
Call
TissCS050, SdCS093, Sd Ct, Peduncle,
PcCS102, Fl bud, Stamen,
Pistil, FlCS107, An
0.05–6.77
ppt, Stem call 0.64 pptCS099,
PetalCS117, FrCS037
Camellia
galactoglucan:
LfCS067
Camellia
polysaccharide:
LfCS122
Camellia
saponin
B, deacyl: LfCS081
Camellia
sinensis polysaccharide TSA: LfCS012
Camellianin A: LfCS108
Camellianin
B: LfCS108
Camelliaside
A: Sd 656–2733.3CS011,CS119
Camelliaside
B: Sd 291–3026.6 CS011,CS119
Camelliaside
C: Sd 2.5CS011
Campesterol:
Sd oilCS134
Carvacrol:
LfCS002
Castasterone:
Lf 7.2 mg/65 kgCS110
Catechin-(4--8)-epi-gallocatechin:
Lf 45.4CS008
Catechin-(4--8)-epi-gallocatechin-3-
gallate:
Lf 45.4CS008
Catechin-(4--8)-epi-gallocatechin-3-
gallate,
epi: Lf 20.8CS008
Catechin,
(+): Lf 0.0017–2.9%CS053,CS049,
Call
TissCS060. St callCS099, ShCS038,
An, StCS099
Catechin,
epi (–): Lf 0.004–6.8%CS053,CS049,
Call
TissCS060, ShCS038, St call 0.07 pptCS099
Catechin,
epi, 3-O-para-hydroxy-benzoate
(–): Lf
3.6CS005
Catechin,
epi, epi-gallo-catechin(4--8)-
3-O-galloyl:
Lf 50CS092
Catechin,
epi-gallo (–), 3-O-paracoumaroate:
Lf 83.3CS140
Catechin,
epi-gallo (–): Lf 3269CS140
Catechin,
epi-gallo, 3-3'-di-O-gallate(–):
LfCS140
Catechin,
epi-gallo, 3-4'-di-O-gallate(–):
LfCS140
Catechin,
epi-gallo, 3-O-gallate (–):
Lf
0.8718%CS140
Catechin,
epi-gallo, gallate(–): St call 0.02
pptCS099, LfCS109
Catechin,
epi-gallo: LfCS140
Catechin-3-O-(3'-O-methyl)-gallate,
epi(–):
Lf 0.08%CS010
Catechin-3-O-(3-O-methyl)-gallate,
epi(–):
Lf 70.6-96.2CS005,CS140
Catechin-3-O-(4-O-methyl)-gallate,
epi(–):
Lf 16CS005
Catechin-3-O-gallate-(4--6)-epigallocatechin-
3-O-gallate,
epi:
Lf 5.8CS008
Catechin-3-
O-gallate-(4--8)-epigallocatechin-
3-O-gallate,
epi: Lf 3.6CS008
Catechin-3-O-gallate,
(+): Lf 0.011%CS084
Catechin-3-O-gallate,
epi(–): Lf 0.0086–
6.6%CS053,CS049
Catechin-gallate,
(+): LfCS082
Catechin-gallate:
LfCS042
Catechol,
(+): PlCS138
Catechol,
epi(–): ShCS128, PlCS138
Catechol,
epi, gallate(–): ShCS128
Catechol,
epi-gallo(–): ShCS128
Catechol,
epi-gallo, gallate(–): ShCS128
Catechol,
gallo, (+): ShCS128
Chasaponin:
PlCS035
Chlorogenic
acid: Call TissCS087, LfCS139
Chondrillasterol:
Sd oilCS130
Citric
acid: LfCS086
Cresol,
meta: LfCS003
Cresol,
ortho: LfCS003
Cresol,
para: LfCS003
Cyclocitral,
: Sh 0.08–0.1%CS100, LfCS002
Cyclohex-2-en-1-4-dione,
2-6-6-trimethyl:
LfCS002
Cyclohex-2-en-1-one,
2-6-6-trimethyl:
LfCS002
Damascenone,
: LfCS002
Damascone,
: LfCS002
Damascone,
: LfCS002
Dammaridienol:
Sd oil 30CS095
Deca-trans-2-cis-4-dien-1-al:
LfCS002
Deca-trans-2-en-1-al:
LfCS002
Dehydrogenase,
NADP-dependent-alcohol:
SdCS031
Demmarenol,
24-methylene: Sd oilCS095
Diphenylamine:
Lf 0.013–1.17%CS098
Dodeca-trans-2-trans-6-10-trien-1-al,
4-ethyl-7-11-dimethyl:
LfCS002
Erucid
acid: Sd oil LfCS134
Ethyl
acetate: LfCS091
Ethyl
lactate: LfCS068
Eugenol:
Fr EOCS030
Euphol:
Sd oilCS095
Farnesene,
, trans-trans: Lf EOCS115
Farnesol:
LfCS091
Fluoride
inorganic: Lf 188CS143
Fluorine,
inorganic: LfCS043
Furan,
2-acetyl: LfCS002
Furan-3-one,
tetrahydro, 2-methyl: LfCS068
Furocoumarin,
angular, 4-hydroxy-2'-
methoxy: LfCS014
Gadoleic
acid: Sd oilCS134
Gallic
acid: LfCS051
Gallocatechin
gallate, (–): Lf 0.188%CS112
Gallocatechin
gallate, (+): LfCS082
Gallocatechin
gallate, epi(–): LfCS125
Gallocatechin
gallate, epi(+): LfCS123
Gallocatechin-(4--8)-epi-catechin:
Lf 36.6CS008
Gallocatechin,
(–): LfCS056
Gallocatechin,
(+): Lf 0.01–12.8%CS053,CS049
Gallocatechin,
epi(+): Lf 1.1%CS083
Gallocatechin,
epi, (–): Lf 0.088-
16.8%CS005,CS049, ShCS038
Gallocatechin,
epi, (4--8)-epi-catechin-
3-)-gallate:
Lf 27.6CS008
Gallocatechin,
epi, 3-O-cinnamate(–):
Lf 13.2CS005
Gallocatechin,
epi, 3-3'-di-O-gallate(–):
Lf 9CS005
Gallocatechin,
epi, 3-4'-di-O-gallate(–):
Lf 9CS005
Gallocatechin,
epi, 3-O-gallate(–):
Lf
0.714%CS005
Gallocatechin,
epi, 3-O-gallate-(4--6)-
epi-catechin-3-O-gallate:
Lf 4.2CS008
Gallocatechin,
epi, 3-O-gallate-(4--8)-
epi-catechin-3-O-gallate:
Lf 44CS008
Gallocatechin,
epi, 3-O-paracoumaroate(–):
Lf 38.4CS005
Gallocatechin,
epi, 8-C-ascorbyl-3-Ogallate:
Lf 11.2CS008
Gallocatechin,
epi: Lf 1.0867%CS101
Gallocatechin-3-5'-di-O-gallate,
epi(–):
Lf
0.06%CS008
Gallocatechin-3-O-(3'-O-methyl)-gallate,
epi(–):Lf
38CS084
Gallocatechin-3-O-gallate
(–): LfCS079
Gallocatechin-3-O-gallate
(+): LfCS157
Gallocatechin-3-O-gallate
(4--8) epicatechin-
gallate,
epi: Lf 0.06%CS010
Gallocatechin-3-O-gallate,
epi(–):
Lf
0.0328–21.3%CS053,CS049, ShCS038
Gallocatechin-3-O-para-coumaroate,
epi
(–): LfCS010
Gallocatechin-gallate,
(–): LfCS042
Gallocateuchin-3-O-gallate,
epi (–):
Lf
5.33%CS010
Galloyl--D-glucose,
1-4-6-tri-O:
Lf
0.01%CS010
Galloylcatechin,
epi (–): LfCS054
Geranic
acid, trans: LfCS002
Geraniol
-D-glucopyranoside: ShCS113
Geraniol:
ShCS113, Lf EO 3.16-25.46%CS136,
LfCS109
Geranyl--primeveroside,
8-hydroxy:
Lf 2.08CS018
Germanicol:
Sd oil 25CS095
Germanicum
inorganic: LfCS120
Gibberellin
A-1: EndospermCS004
Gibberellin
A-19: EndospermCS004
Gibberellin
A-20: EndospermCS004
Gibberellin
A-3, iso: EndospermCS004
Gibberellin
A-3: EndospermCS004
Gibberellin
A-38: EndospermCS004
Gibberellin
A-44: EndospermCS004
Gibberellin
A-8: EndospermCS004
Gibberellin
A-S: EndospermCS004
Glucogallin,
: Lf 28.4CS008
Glucose,
-D, 1-0-galloyl-4-6-(–)-
hexahyroxy-diphenoyl:
Lf 30CS092
Glucose,
-D, 1-4-6-tri-O-galloyl: Lf 5CS092
Glutamic
acid: N-para-coumaryl: LfCS133
Heptan-1-al:
Sh 0.02–0.03%CS100
Heptan-2-ol:
LfCS068
Heptan-2-one,
5-iso-propyl: LfCS002
Heptan-2-one:
LfCS002
Heptan-3-ol:
LfCS068
Hepta-trans-2-trans-4-dien-1-al:
Sh
0.06–0.1%CS100
Hept-trans-2-en-1-al:
LfCS002
Hex-1-en-3-ol:
LfCS068
Hex-2-en-1-al,
5-methyl-2-phenyl: LfCS002
Hex-5-en-4-olide,
4-methyl: LfCS002
Hexadecane,
N: LfCS091
Hexan-1-al:
ChloroplastCS129,
Sh
0.55–1.03%CS100
Hexan-1-ol,
2-ethyl: LfCS002
Hexan-2-ol:
LfCS068
Hexa-trans-2-cis-4-dien-1-al:
LfCS002
Hex-cis-3-en-1-al:
Lf 370CS034
Hex-cis-3-en-1-ol
acetate: LfCS091
Hex-cis-3-en-1-ol
butyrate: LfCS091
Hex-cis-3-en-1-ol
caproate: LfCS091
Hex-cis-3-en-1-ol
formate: LfCS002
Hex-cis-3-en-1-ol
hexanoate:
Sh
0.02–0.03%CS100
Hex-cis-3-en-1-ol
hex-trans-2-enoate:
LfCS002
Hex-cis-3-en-1-ol
propionate: LfCS002
Hex-cis-3-en-1-ol,
-D-glucoside: LfCS076
Hex-cis-3-en-1-ol:
LfCS025, Lf EO 2.15–
15%CS136, Sh 0.09–0.13%CS100
Hex-trans-2-en-1-al:
LfCS065, Lf EO 1.13–
25.48%CS136, Sh 2.09–3.1%CS100
Hex-trans-2-en-1-ol:
Sh 0.04–0.06%CS100
Hex-trans-2-enyl
acetate: LfCS002
Hex-trans-2-enyl
butyrate: LfCS002
Hex-trans-2-enyl
formate: LfCS002
Hex-trans-2-enyl
hexanoate: LfCS002
Hex-trans-2-enyl
propionate: LfCS002
Hex-trans-3-enyl
butyrate: LfCS002
Hex-trans-3-enyl
hex-cis-3-enoate: LfCS002
Hex-trans-3-enyl
propionate: LfCS002
Hex-trans-3-enyl-2-methyl
butyrate: LfCS002
Hexyl
butyrate: LfCS002
Hexyl
formate: LfCS002
Hyperoside:
LfCS058
Indole:
LfCS109
Indole-3-methyl-ethanolate:
LfCS015
Inositol,
myo, 2-O--L-arabinopyranosyl:
Lf 0.4%CS116
Inositol,
myo, 2-O--L-arabinopyranoside:
Lf 0.4%CS106
Inositol,
myo, 2-O--L-arabinoside: LfCS077
Ionone,
: Sh 0.03–0.05%CS100, LfCS068
Ionone,
, 1'-2'-dihydro, 1'-2'-epoxy:
Lf EOCS132
Ionone,
, 1'-2'-dihydroxy, 1'-2'-threo:
Lf EOCS132
Ionone,
, 3'-oxo: Lf EOCS132
Ionone,
: Lf EO 0.02–0.31%CS136,
Sh
0.17–0.29%CS100
Jasmonate,
dihydro, methyl-trans: LfCS002
Jasmone,
cis: Lf EO 0.05–0.2%CS136
Jasmone:
LfCS091
Jasmonic
acid, (1R, 2R), (–): LfCS080
Jasmonic
acid, (1R, 2S), (+): LfCS080
Jasmonic
acid: PollenCS137, AnCS137, LfCS091
Kaempferitin:
LfCS139
Kaempferol:
LfCS026, ShCS094
Kaempferol-3-O-galactosyl-rhamnosylglucoside:
LfCS058
Kaempferol-3-O-glucosyl(1-3)rhamnosyl
(1-6)galactoside:
LfCS009
Kaempferol-3-O-glucosyl-rhamnoside:
LfCS058
Kaempferol-3-O-glucosyl-rhamnosyl-galactoside:
LfCS058
Lauric
acid: Sd oilCS134
Ligustrazine:
LfCS027
Limonene:
LfCS068
Linalool
-D-glucopyranoside: ShCS113
Linalool
oxide A: LfCS091
Linalool
oxide B: LfCS091
Linalool
oxide C: LfCS091
Linalool
oxide I: LfCS077
Linalool
oxide II: LfCS077
Linalool
oxide III: LfCS077
Linalool
oxide IV: LfCS077
Linalool
oxide: Headspace volatileCS044
Linalool,
(R): LfCS074
Linalool,
cis, oxide (furanoid): LfCS074
Linalool,
cis, oxide (pyranoid): LfCS074
Linalool,
cis, oxide: Sh 0.06–0.16%CS100
Linalool,
trans, oxide (furanoid): LfCS074
Linalool,
trans, oxide (pyranoid): LfCS074
Linalool,
trans, oxide: Lf EO 3.18–
4.23%CS136, Sh 0.15–0.43%CS100
Linalool:
LfCS121, Headspace volatileCS044,
ShCS113, Lf EO 8.2–19.84CS136
Linoleic
acid: Sd oilCS134, LfCS069
Linolenic
acid: LfCS069
Loliolide:
Lf EOCS132
Lupeol:
Sd oilCS062
Malic
acid: LfCS086
Malonic
acid: LfCS086
Menthol:
LfCS068
Methionine,
S-methyl: Lf 7–24.5 mg%CS158
Methylamine:
Lf 50CS141
Morine:
LfCS045
Myrcene:
LfCS091
Myricetin:
LfCS026
Myristic
acid: Sd oilCS134, LfCS069
Naringenin:
ShCS094
Naringenin-fructosyl-glucoside:
LfCS063
Neral:
LfCS002
Nerolidol:
LfCS109, Sh 0.08–0.12%CS100
NH3 inorganic: Lf 400CS141
Nicotiflorin:
LfCS133
Nicotine:
Lf 15.5 ng/gCS047
Nonal-1-al:
Sh 0.04–0.06%CS100
Nonal-2-ol:
LfCS068
Nonan-2-one:
LfCS002
Nona- trans-2-cis-4-dien-1-al:
LfCS002
Nona- trans-2-cis-6-dien-1-al:
LfCS002
Nona-trans-2-en-1-al:
LfCS002
Nona-trans-2-trans-4-dien-1-al:
LfCS002
Oct-1-en-3-ol:
LfCS068
Octa-1-5-7-trien-3-ol,
3(S)-7-dimethyl:
Lf EOCS132
Octa-1-5-diene-3-7-diol,
3(S)-7-dimethyl,
(+): Lf
EOCS132
Octan-2-one:
LfCS002
Octan-3-ol:
LfCS068
Octanoate,
ethyl: LfCS002
Octanoate,
methyl: LfCS002
Octa-trans-2-cis-4-dien-1-al:
LfCS002
Octa-trans-2-trans-4-dien-1-al:
LfCS002
Octa-trans-3-cis-5-dien-2-one:
LfCS002
Oct-trans-2-enoic
acid: LfCS002
Oleic
acid: Sd oilCS134, LfCS069
Oolonghomobisflavan
A: Lf 10.6CS008
Oolonghomobisflavan
B: Lf 7.2CS008
Oolongtheanin:
Lf 1.8CS006
Oxalic
acid: Lf 1.0%CS144
Palmitic
acid: Sd oilCS134, LfCS069
Pedunculagin:
LfCS041
Pent-1-en-3-ol:
LfCS068, Sh 0.21–0.23%CS100
Pent-2-en-1-al,
4-methyl-2-phenyl: LfCS002
Pentadecane,
2-6-10-14-tetramethyl: LfCS091
Pentan-1-ol:
Sh 0.06–0.11%CS100
Pentan-2-ol,
methyl: LfCS068
Pentan-3-ol,
methyl: LfCS068
Pentanoic
acid: 2-amino-5-(N-ethylcarboxamido):
Lf 120CS105
Pent-cis-2-en-1-ol:
Sh 0.1-0.14%CS100
Pent-cis-3-en-1-al:
LfCS002
Phenol:
LfCS003
Phenyl,
acetate, ethyl: LfCS002
Phenyl,
acetate, hexyl: LfCS002
Phenylacetic
acid: LfCS002
Phenylethanol,
2: LfCS091
Phenylethyl
alcohol, 2: Sh 0.1–0.13%CS100
Phenylethyl
alcohol: Headspace
volatileCS044
Pheophytin
A: LfCS088
Pheophytin
B: LfCS088
Pinene,
a: LfCS068
Pipecolic
acid, L: FrCS030
Pipecolic
acid: LfCS037, FrCS037
Polysaccharide
T-B: LfCS111
Procyanidin
B-2 3'-O-gallate: Lf 166.7CS140
Procyanidin
B-2, 3-3'-di-O-gallate: Lf
0.00084–0.13%CS008,CS010
Procyanidin
B-2: Lf 5.8CS008
Procyanidin
B-3, 3-O-gallate: LfCS070
Procyanidin
B-3: Lf 0.21%CS010
Procyanidin
B-4, 3'-O-gallate: Lf 141CS140
Procyanidin
B-4: Lf 46.6CS008
Procyanidin
B-5, 3-3'-di- O-gallate: Lf 2.6CS008
Procyanidin
C-1: LfCS010
Prodelphinidin
A-2, 3'-O-gallate: Lf 4.4CS008
Prodelphinidin
B-2, 3'-O-gallate: Lf 238CS008
Prodelphinidin
B-2, 3-3'-di-O-gallate:
Lf 18.4CS008
Prodelphinidin
B-2,3'-O-gallate: Lf 147.4CS140
Prodelphinidin
B-4, 3'-O-gallate:
Lf
63.8–1200CS008,CS010
Prodelphinidin
B-4: Lf 56.8–800CS008,CS010
Prodelphinidin
B-5, 3-3'-di-O-gallate:
Lf 29.8CS008
Proline,
hydroxy: LfCS037, FrCS037
Propionamide,
N-ethyl: LfCS027
Propiophenone,
2-4-dimethyl: LfCS027
Propiophenone,
para-ethyl: LfCS027
Prunasin:
LfCS059
Pyrazine,
2-3-dimethyl: LfCS027
Pyrazine,
2-5-dimethyl: LfCS027
Pyrazine,
2-6-dimethyl: LfCS027
Pyrazine,
2-ethyl-3-5-dimethyl: LfCS027
Pyrazine,
2-ethyl-3-6-dimethyl: LfCS036
Pyrazine,
2-ethyl-5-methyl: LfCS027
Pyrazine,
2-ethyl-6-methyl: LfCS027
Pyrazine,
ethyl: LfCS027
Pyrazine,
methyl: LfCS027
Pyrazine,
trimethyl: LfCS027
Pyridine,
2-5-dimethyl: LfCS027
Pyridine,
2-6-dimethyl: LfCS027
Pyridine,
2-acetyl: LfCS036
Pyridine,
2-ethyl: LfCS027
Pyridine,
2-ethyl-5-methyl: LfCS036
Pyridine,
2-ethyl-6-methyl: LfCS036
Pyridine,
2-methyl: LfCS027
Pyridine,
2-phenyl: LfCS027
Pyridine,
3-ethyl: LfCS027
Pyridine,
3-methoxy: LfCS036
Pyridine,
3-methyl: LfCS027
Pyridine,
3-N-butyl: LfCS036
Pyridine,
3-phenyl: LfCS027
Pyridine,
4-methyl: LfCS027
Pyridine,
4-vinyl: LfCS036
Pyridine:
LfCS027
Quercetin:
LfCS026, ShCS094
Quercetin-3-glucosyl(1-3)rhamnosyl
(1-6)galactoside:
LfCS009
Quercetin-fructosyl-glucoside:
LfCS063
Quercimeritrin:
LfCS026
Quercitrin,
iso: LfCS133
Quercitrin:
LfCS058
Quinic
acid, (–): LfCS104
Quinoline,
2-4-dimethyl: LfCS027
Quinoline,
2-6-dimethyl: LfCS027
Quinoline,
2-methyl: LfCS036
Quinoline,
3-N-butyl: LfCS027
Quinoline,
3-N-propyl: LfCS027
Quinoline,
4-8-dimethyl: LfCS027
Quinoline,
6-methyl: LfCS036
Rutin:
LfCS058
Safranal:
LfCS002
Safrole:
LfCS002
Salicylic
acid: Headspace volatileCS044
Sesquiphelandrene,
b: LfCS109
Sitosterol,
: Sd oilCS134
Spinasterol,
22-23-dihydro: Sd oilCS131
Spinasterol,
, -D-glucoside: RtCS039
Spinasterol,
: RtCS039
Spinasterol:
Sd oilCS131
Spinasterone,
22-23-dihydro: Sd oilCS131
Spinasterone:
Sd oilCS131
Stearic
acid: Sd oilCS134
Stigmasterol:
Sd oilCS134
Strictinin:
Lf 0.01%CS010
Succinic
acid: LfCS086
Tannic
acid: Lf CS126
Tannin:
LfCS024
Taraxasterol,
Pseudo: Sd oilCS095
Taraxerol:
Sd oil 20CS095
Tartaric
acid: LfCS086
Tea
polysaccharides: LfCS055
Teasaponin
B-1: LfCS057
Teasaponin
B-2: LfCS040
Teasaponin
B-3: LfCS040
Teasaponin
B-4: LfCS040
Teasterone:
LfCS090
Tectoquinone:
RtCS039
Terpineol,
4: LfCS002
Terpineol,
: Sh 0.07–0.1%CS100, LfCS068
Theacitrin
A: Lf 0.08%CS016
Theaflagallin,
epi, 3-O-gallate: Lf 17CS008
Theaflagallin-3-O-gallate,
epi: Lf 0.02%CS010
Theaflavate
B: LfCS019
Theaflavic
acid, epi, gallate: LfCS064
Theaflavic
acid, epi: LfCS064
Theaflavin,
digallate: LfCS071
Theaflavin,
iso: 3'-O-gallate: Lf 25CS019
Theaflavin,
monogallate A: LfCS071
Theaflavin,
monogallate B: LfCS071
Theaflavin,
monogallate: LfCS124
Theaflavin,
neo: 3-O-gallate: Lf 30CS019
Theaflavin:
LfCS046, Sh 1.12–1.40%CS100,
FlCS159
Theaflavin-3'-gallate:
LfCS046
Theaflavin-3'-O-gallate:
FlCS159,
Lf
18.6–800CS008,CS010
Theaflavin-3-3'-
digallate: FlCS159
Theaflavin-3-3'-di-O-gallate:
Lf
18.2–300CS008,CS010
Theaflavin-3-gallate:
LfCS046
Theaflavin-3-O-gallate:
FlCS159,
Lf
6-700CS008,CS010
Theaflavin-monogallate
A: LfCS085
Theaflavin-monogallate
B: LfCS085
Theaflavonin,
degalloyl: Lf 17.5CS010
Theaflavonin:
Lf 11.5CS010
Theanaphthoquinone:
LfCS023
Theanine:
LfCS052, Call TissCS066, Seedling Rt
109, Sh
63, Cy 577 mg%CS097, St Call
0.37
ppt, An 1.6-2.9%, St 34.9 pptCS099
Thearubigin: Sh
13.56–15.74%CS100, LfCS139
Theasapogenol
A, 22-O-angeloyl: SdCS020
Theasapogenol
B, 22-O-angeloyl: SdCS020
Theasapogenol
E, 22-O-angeloyl: SdCS020
Theasaponin
B-1: LfCS081
Theasaponin
E-1: Sd 75CS017
Theasaponin
E-2: Sd 10CS017
Theasaponin,
gluco: SdCS061
Theasaponin:
SdCS127, LfCS142
Theasinensin
A: Lf 0.01866–4.8718%CS006,CS140
Theasinensin
B: Lf 128.2–600CS140,CS010
Theasinensin
C: Lf 70.2CS006
Theasinensin
D: Lf 17.6CS006
Theasinensin
E: Lf 14.4CS006
Theasinensin
F: Lf 19.6CS006
Theasinensin
G: Lf 8CS006
Theaspirane,
dihydro, 6-7-epoxy: LfCS002
Theaspirane,
dihydro, 6-hydroxy: LfCS002
Theaspirane:
LfCS002
Theaspirone:
Lf EOCS132
Theobromine:
LfCS029, Call TissCS050, Sd,
PcCS102, Fl Bd, FlCS107, Petal, Pistil,
StamenCS117, An, St, St CallCS099, PlCS033,
SeedcoatCS102
Theogallin:
Lf 6-55.5CS008,CS010
Theophylline:
SdCS093
Thiazole,
2-4-5-trimethyl: LfCS036
Thiazole,
2-4-dimethyl: LfCS036
Thiazole,
2-4-dimethyl-4-ethyl: LfCS036
Thiazole,
2-5-dimethyl: LfCS036
Thiazole,
5-methyl: LfCS036
Thymol:
LfCS002
Tirucalla-7-24-dien-3--ol,
5-:
Sd oil
12CS062
Tirucalla-7-24-dien-3--ol:
Sd oilCS095
Tirucallol:
Sd oilCS095
Toluidine,
ortho: LfCS027
Triacontan-1-ol:
LfCS075
Tricetin:
ShCS094
Tricetinidin:
LfCS139
Trifolin:
LfCS058
Tr-saponin
A: Rt 2.2CS022
Tr-saponin
B: Rt 5.9CS022
Tr-saponin
C: Rt 2.8CS022
Typhasterol:
LfCS090
Umbelliferone:
LfCS032
Undeca-2-one,
6-10-dimethyl: LfCS002
Undeca-trans-2-en-1-al:
LfCS002
Urea:
PlCS033
Vitamin
K-1: Lf 3.1-16.5CS072,
Vitexin,
iso, 2''-O-glucoside: LfCS103
Vitexin:
ShCS096
Vomifeliol, dehydro:
Lf EOCS132
PHARMACOLOGICAL ACTIVITIES AND CLINICAL TRIALS (Ross, I. A.
2005)
Antibacterial
activity. Alcohol extract of black tea, assayed on Salmonella typhi and
Salmonella paratyphi A, was active on all strains of Salmonella
paratyphi A, and only 42.19% of Salmonella typhi strains were inhibited by the
extractCS048. Hot water extract of the dried entire plant and the tannin fraction,
on agar plate, were active on Escherichia coli, Pseudomonas
aeruginosa, and Staphylococcus aureusCS160.
Anticancer activity.
Catechin,
administered to pheochromocytoma cells in cell culture, was active. The cells
were incubated with different concentrations of catechin at short-term (2 days)
and long-term (7 days) in Dulbecco’s modified Eagle medium. The activity of superoxide
dismutase was measured and its mRNA assayed by Northern blotting. After
incubation for 2 days, catechin significantly increased the activity of copper/zinc
superoxide dismutase. However, it did not produce significant effect at 7 days.
The magnesium superoxide dismutase activity produced significant changes in
both short- and long-term treatment groups. The amount of mRNA also showed
similar changesCS040.
Anticarcinogenic
activity. The anticarcinogenic activity of tea phenols has been demonstrated
in rats and mice transplantable tumors, carcinogen-induced tumors in digestive
organs, mammary glands, hepatocarcinomas, lung cancers, skin tumors, leukemia, tumor
promotion, and metastasis. The mechanisms of this effect indicated that the
inhibition of tumors may be the result of both extracellular and intracellular mechanisms
indicating the modulation of metabolism, blocking or suppression, modulation of
DNA replication and repair effects, promotion, inhibition of invasion and metastasis,
and induction of novel mechanismsCS002. The association
of green tea and cancer has been investigated in 8552 Japanese women 40 years
of age. After 9 years of follow-up study, 384 cases of cancer were identified.
There was a negative association between cancer incidence and green tea consumption,
especially among females consuming more than 10 cups of tea a day. A slow down
in increases of cancer incidence with age was observed among females who
consumed more than 10 cups dailyCS010. Tea, taken by lung cancer patients
at a dose of two or more cups per day, reduced the risk by 95%. The protected effect
was more evident among Kreyberg I tumors (squamous cell and small cells) and among
light smokersCS011. The green tea polyphenols, epi-gallocatechin-3-gallate,
applied topically to human skin, prevented penetration of ultraviolet (UV)
radiation. This was demonstrated by the absence of immunostaining for
cyclobutane pyrimidine dimers in the reticular dermis. Topical administration
to the skin of mice inhibited UVB-induced infiltration of CDIIb+cells. The treatment
also results in reduction of the UVB-induced immunoregulatory cytokine
interleukin (IL)-10 in the skin and draining lymph nodes, and an elevated amount
of IL-12 in draining lymph nodesCS015. Green tea extract, in human umbilical
vein endothelial cells, did not affect cell viability but significantly reduced
cell proliferation dose-dependently and produced a dose-dependent accumulation
of cells in the gastrointestinal phase. The decrease of the expression of
vascularendothelial growth factor receptors fms-like tyrosine kinase and fetal
liver kinase-I/ kinase insert domain containing receptor in the cell culture by
the extract was detected with immunohistochemical and Western blotting methodsCS020. Green and black
tea, administered orally to hairless mice in the absence of any chemical
initiators or promoters, resulted in significantly fewer skin papillomas and
tumors induced by UVA and UVB light. Black tea however, provided better
protection against UVB-induced tumors than green tea. Black tea consumption was
associated with a reduction in the number of sunburn cells in the epidermis of mice
24 hours after irradiation, although there was no effect of green tea. Other
indices of early damage such as necrotic cells or mitotic figures were not
affected. Neutrophil infiltration as a measure of skin redness was slightly
lowered by tea consumption in the UVB groupCS023.
Epigallocatechin-3-gallate, in cell culture, activated proMMP-2 in U-87 glioblastoma
cells in the presence of concanavalin A or cytochalasin D, two potent activators
of MT1-MMP, resulted in proMMP-2 activation that was correlated with the cell
surface proteolytic processing of Mt1-MMP to it’s inactive 43 kDa form. Addition
of epigallocatechin-3-gallate strongly inhibited the MT1-MMP-driven migration
in the cells. The treatment of cells with non-cytotoxic doses of
epigallocatechin-3-gallate significantly reduced the amount of secreted pro
MMP-2, and led to a concomitant increase in intracellular levels of that protein.
The effect was similar to that observed using well-characterized secretion inhibitors
such as brefeldin A and manumycin, indicative that epigallocatechin could also
potentially act on intracellular secretory pathwaysCS044. Green tea polyphenols,
at a dose of 30 mg/mL, inhibited the photolabeling of P-glycoprotein (P-gp) by
75% and increased the accumulation of rhodamine-123 in the multidrug-resistant
cell line CH(R)C5. This result indicated that green tea polyphenols interact with
P-gp and inhibited its transport activity. The modulation of P-gp was a reversible
process. Epigallocatechin-3-gallate potentiates the cytotoxicity of vinblastine
in CH(R)C5 cells. The inhibitory effect on P-gp was also observed in human Caco-2
cellsCS045.
Anticataract
activity. Tea, administered in culture to enucleated rat lens, reduced the
incidence of selenite cataract in vivo. The rat lenses were randomly divided
into normal, control and treated groups and incubated for 24 hours at 37oC.
Oxidative stress was induced by sodium selenite in the culture medium of the
two groups (except the normal group). The medium of the treated group was
additionally supplemented with tea extract. After incubation, lenses were subjected
to glutathione and malondialdehyde estimation. Enzyme activity of superoxide
dismutase, catalase, and glutathione peroxidase were also measured in different
sets of the experiment. In vivo cataract was induced in 9-day-old rat pups of
both control and treated groups by a single subcutaneous injection of sodium selenite.
The treated pups were injected with tea extract intraperitoneally prior to selenite
challenge and continued for 2 consecutive days thereafter. Cataract incidence was
evaluated on 16 postnatal days by slit lamp examination. There was positive modulation
of biochemical parameters in the organ culture study. The results indicated that
tea act primarily by preserving the antioxidant defense systemCS039.
Antidiarrheal
activity. Hot water extract of tea, administered orally to rats, was
effective in all the models of diarrhea used. Naloxone (0.5 mg/kg, ip) and
loperamide significantly inhibited the antidiarrheal activity of the extractCS029.
Antifungal
activity. Ethanol (50%) extract of the entire plant, in broth culture at a
concentration of 1 mg/mL, was inactive on Aspergillus fumigatus and Trichophyton
mentagrophytesCS161. Hot water extract of the leaf on agar plate at a concentration
of 1.0% was active on Alternaria tenuis, Pythium aphanidermatum, and
Rhizopus stoloniferCS162. Saponin fraction of the leaf on agar plate was active on Microsporum
audonini, minimum inhibitory concentration (MIC) 10 mg/mL; Epidermophyton
floccosum and Trichophyton mentagrophytes, MICs 25 g/mLCS165.
Antihypercholesterolemic
activity. Tea supplemented with vitamin E, administered to male Syrian
hamsters, reduced plasma low-density lipoprotein (LDL) cholesterol concentrations,
LDL oxidation, and early atherosclerosis compared to the consumption of tea
alone by the hamsters. The antioxidant action of vitamin E is through the incorporation
of vitamin E into the LDL molecule. The hamsters were fed a semipurified hypercholesterolemic
diet containing 12% coconut oil, 3% sunflower oil, and 0.2% cholesterol
(control), control and 0.625% tea, control and 1.25% tea or control and 0.044% tocopherol
acetate for 10 weeks. The hamsters fed the vitamin E diet compared to the
different concentrations of tea significantly lower plasma LDL cholesterol concentrations,
–18% (p < 0.007), –17% (p < 0.02), and –24% (p <
0.0001), respectively. Aortic fatty streak areas were reduced in the vitamin E
diet group compared to the control, –36% (p < 0.04) and low tea –45%
(p < 0.01) diets. Lag phase of conjugated diene production was
greater in the vitamin E diet compared to the control, low tea, and high tea
diets, 41% (p < 0.0004), 40% (p < 0.0004), and 39% (p <0.0008),
respectively. Rate of conjugated diene production was reduced in the vitamin E
diet compared to the control, low tea, and high tea diets, –63% (p <
0.002), –57% (p < 0.005), and –59% (p < 0.02), respectivelyCS005. Infusion of black
tea leaves was taken by 31 men (ages 47 14) and 34 females (ages 35
13) in a 4-week study. Six mugs of tea were taken daily vs placebo (water,
caffeine, milk, and sugar) and blood lipids, bowel habit, and blood pressure
measured during a run-in period and at the end weeks 2, 3, and 4 of the test period.
Compliance was established by adding a known amount of p-aminobenzoic
acid to selected tea bags and then measure it excretion in the urine. Mean
serum cholesterol values during run-in, placebo and on tea drinking were 5.67
1.05, 5.76 1.11, and 5.69 1.09 mmol/L (p = 0.16).
There were also no significant changes in diet, LDL-cholesterol, high-density
lipoprotein (HDL) cholesterol, triacylglycerols, and blood pressure in the tea
intervention period compared with placebo. Stool consistency was softened with
tea compared with the placebo, and no other differences were observed in bowel
habit. The results were unchanged within 15 “noncompliers” whose p-aminobenzoic
acid excretion indicated that fewer than six tea bags had been used, were
excluded from the analysis, and when differenced between run-in and tea periods
were considered separately for those who were given tea first or secondCS167.
Anti-inflammatory
effect. Epigallocatechin- 3-gallate was shown to mimic its antiinflammatory
effects in modulating the IL-I -induced activation of mitogen
activated protein kinase in human chondrocytes. It inhibited the IL-I -induced
phosphorylation of c-Jun N-terminal kinase (JNK) isoforms, accumulation of
phosphoc- Jun and DNA-binding activity of AP-1 in osteoarthritis chondrocytes,
IL-I but not epigallocatechin-3-gallate, and induced the expression
of JNK p46 without modulating the expression of JNK p54 in osteoarthritis chondrocytes.
In immune complex kinase assays, epigallocatechin-3-gallate completely blocked
the substrate phosphorylating activity of JNK but not p38-mitogen activated
protein kinase (MAPK). Epigallocatechin-3-gallate had no inhibitory effect on
the activation of extracellular signalregulated kinase p44/p42 (ERKp44/p42) or p38-MAPK
in chondrocytes. Epigallocatechin-3-gallate did not alter the total nonphosphorylated
levels of either p38- MAPK or ERKp44/p42 in osteoarthritis chondrocytesCS033.
Epigallocatechin-3-gallate administered to primary human osteoarthritis chondrocytes
at a concentration of 100 M in cell Culture, inhibited
the IL-I -induced production of nitric oxide by interfering with the
activation of nuclear factor (NF)BCS042. Tea, in culture
with bovine nasal and metacarpophalangeal cartilage and human nondiseased
osteoarthritis and rheumatoid cartilage with and without reagents known to
accelerate cartilage matrix breakdown, produced chondroprotective effect that
may be beneficial for the arthritis patient by reducing inflammation and the
slowing of cartilage breakdown. Individual catechins were added to the cultures
and the amount of released proteoglycan and type II collagen were measured by
metachromatic assay and inhibition enzyme-linked immunosorbent assay (ELISA),
respectively. Possible nonspecific or toxic effects of the catechins were assessed
by lactate output and proteoglycan synthesis. Catechins, particularly those containing
a gallate ester, were effective at micromolar concentrations at inhibiting proteoglycan
and type II collagen breakdownCS043.
Antimutagenic
activity. The anticarcinogenic activity of tea phenols has been demonstrated
in rats and mice, transplantable tumors, carcinogen-induced tumors in digestive
organs, mammary glands, hepatocarcinomas, lung cancers, skin tumors, leukemia, tumor
promotion, and metastasis. The mechanisms of this effect indicated that the
inhibition of tumors maybe the result of both extracellular and intracellular mechanisms
indicting the modulation of metabolism, blocking or suppression, modulation of
DNA replication and repair effects, promotion, inhibition of invasion and Metastasis, and
induction of novel mechanismsCS002. Green and black teas, administered orally
to human adults, were effective. Between 60 and 180 minutes after the teas were
administered, the antimutagenic active compounds were recovered from the jejunal
compartment by means of dialysis. The dialysate appeared to inhibit the
mutagenicity of the food mutagen 2-amino-3,8- dimethylimidazo[4,5-f]quinoxaline
on Salmonella typhimurium. The maximum inhibition was measured at 2
hours after administration and was comparable for black and green teas. The
maximum inhibition observed with black tea was reduced by 22, 42, and 78% in
the presence of whole milk, semi-skimmed milk, and skimmed milk, respectively.
Whole milk and skimmed milk abolished the antimutagenic activity of green tea by
more than 90% and semiskimmed milk by more than 60%. When a homogenized
breakfast was taken with black tea, the antimutagenic activity was eliminated. When
tea and mutagen 2-amino-3,8- dimethylimidazo[4,5-f]quinoxaline were added to
the system, 2-amino-3,8-dimethylimidazo[ 4,5-f]quinoxaline mutagenicity was efficiently
inhibited, with green tea showing a slightly stronger antimutagenic activity than
black tea. The addition of milk had only a small inhibiting effect on the antimutagenicity.
The antimutagenic activity corresponded with reduction in antioxidant capacity
and with a decrease of concentration of catechin, epigallocatechin gallate, and
epigallocatechinCS014. Chinese white tea, tested on rat liver S9 in assay for methoxyresorufin
O-demethylase, inhibited methoxyresorufin O-demethylase activity and
attenuated the mutagenic activity of 3-methylimidazo[4,5-f]quinoline (IQ) in absence
of S9. Nine of the major constituents found in green and white teas were mixed
to produce artificial teas according to their relative levels in white and
green teas. The complete tea exhibited higher antimutagenic potency compared
with the corresponding artificial teaCS019. Green and black tea
polyphenols, applied to the surfaces of ground beef before cooking, inhibited
the formation of the mutagens in a dose-related fashionCS025. Green or black
tea polyphenols sharply decreased the mutagenicity of a number of aryl- and
heterocyclic amines, of aflatoxin B1, benzo[a]pyrene,
1,2-dibromoethane, and more selectively of 2-nitropropane, all involving an
induced rat liver S9 fraction. Good inhibition was found with two nitrosamines
that required a hamster S9 fraction for biochemical activation. No effect was
found with 1-nitropyrene and with the direct-acting (no S9) 2-chloro-4-methyl-thiobutanoic
acidCS027. Hot water extract on the leaf was evaluated in cell cultures on
various systems vs decaffeinated and caffeinated teas. On mouse mammary gland
vs decaffeinated and caffeinated teas, ICs50 were 10 mg/mL and
10 g/mL on CAA427, IC50 27 mg/mL and 31 g/mL, and on
epithelial cells, IC50 0.01 ng/mL and 0.3 ng/mLCS169. Hot water extract of the leaf, on agar plate at a concentration
of 1 mg/ plate, was active on Salmonella typhimurium TA98 vs 2-amino-3
methylimidazo [4,5-f]quinoline-induced mutagenesis and produced weak activity
vs benzo[a]pyreneinduced mutagenesisCS168. Infusion of the leaf, on agar plate at a concentration of 0.7 mg/plate,
was active on Salmonella typhimurium TA98 and TA100 vs 2-amino-3-m e t h
y l i m i d a z o [ 4 , 5 - f ] q u i n o l i n e - ; 3-amino-1,4-dimethyl-5H-pyrid[4,3-b]indole(Trp-1);
aflatoxin B1-; 2-amino-6-methyl-dipyrido[1,2-A:3,2-d]imidazole-, and
benzo[a]pyrene-induced carcinogenesisCS170. Infusion of the leaf, on agar plate at a concentration of 50
mg/plate, was active on Salmonella typhimurium TA98 vs 2-amino-3-methylimidazo[4,5-f]quinoline-;
2-amino-3,4-dimethyl-imidazo[4,5- f]quinoline-;2-amino-3,8-dimethylimid a z o [
4 , 5 - f ] q u i n o x a l i n e - ; 2-amino-1-methyl-6-phenylimidazo[4,5-b]-p
y r i d i n e - ; 2 - a m i n o - 3 , 7 , 8 - trimethylimidazo[4,5-f]quinoxaline-;
2-amino-3,4,7,8-tetramethyl-3H-imidazo- [4,5-f]quinoxaline-inoxaline-; 3-amino-1,4-d
i m e t h y l - 5 H - p y r i d [ 4 , 3 - b ] i n d o l e (Trp-P-I)- and
3-amino-1-methyl-5Hpyrido [4,3-b]indole-induced mutagenesis. Metabolic activation
was required for positive resultsCS171.
Anti-neoplastic
effect. Green tea, administered orally at a dose of 6 g per day in six doses
to 42 patients who were asymptomatic and had manifested, progressive prostate specific
antigen elevation with hormone therapy, produced limited antineoplastic activity.
Continued use of luteinizing hormone-releasing hormone agonist was permitted.
However, patients were ineligible if they had received other treatments for their
disease in the preceding 4 weeks or if they had received a long-acting antiandrogen
therapy in the preceding 6 weeks. The patients were monitored monthly for
response and toxicity. Tumor response, defined as a decline of 50% or greater
in the baseline prostate-specific antigen (PSA) value, occurred in a single patient,
or 2% of The cohort (95% confidence interval [CI], 1–14%). This one response
was not sustained beyond 2 months. At the end of the first month, the median
change in the PSA value from baseline for the cohort increased by 43%CS031. Infusion of the
leaf, administered in the drinking of female mice at a concentration of 1.25%,
was active vs UV radiation-induced papillomas and tumorsCS172. Leaves in the
drinking water of female mice at a dose of 0.6% reduced lung tumor multiplicity
and volume in 4-(methylnitrosamine)-1-(3-pyridyl)-1-butanone (NNK) treated miceCS173.
Antioxidative
effect. Tea, administered orally to rats, decreased the thiobarbituric acid
reactive substances (TBARS) contents in urine and lowered the esterified and
total cholesterol contents in plasma as compared with a control group. TBARS
contents in liver, plasma, and cholesterol levels in the liver were not
affected. The lower plasma cholesterol concentration could not be explained by
increased fecal excretion of cholesterol or bile acids. On the other hand, a
relationship between decreased plasma cholesterol and significantly higher
acetate concentrations in the cecum, colon, and portal blood of rats was
assumed. Copper absorption was significantly increased while iron absorption
was not affectedCS007. Epigallocatechin gallate, tea polyphenols, and tea extract
were added to human plasma and lipid peroxidation induced by the water-soluble
radical generator 2,2'-azobis (2-amidinopropane) dihydrochloride. Following a
lag phase, lipid peroxidation was initiated and it occurred at a rate that was lower
in a dose that was lowered in a dosedependent manner by the polyphenols. Similarly,
epigallocatechin gallate and the extract added to plasma strongly inhibited 2 ,
2 ' - a z o b i s ( 2 - a m i d i n o p r o p a n e ) dihydrochloride-induced
lipid peroxidation. The lag phase preceding detectable lipid peroxidation was
the result of the antioxidant activity of endogenous ascorbate, which was more
effective at inhibiting lipid peroxidation than the tea polyphenols and was not
spared by these compounds. When eight volunteers consumed the equivalent of six
cups of tea, the resistance of their plasma to lipid peroxidation did not increase
over a period of 3 hoursCS009. Black tea leaves, administered to human red blood cells, was
effective against damage by oxidative stress induced by inducers such as phenylhydrazine,
Cu2+-ascorbic acid, and xanthine/xanthine oxidase systems. Lipid peroxidation
of pure erythrocyte membrane and of whole red blood cell was completely prevented
by black tea extract. Similarly, the tea provided total protection against degradation
of membrane proteins. Membranefluidity studies as monitored by thefluorescent
probe 1,6-diphenyl-hexa-1,3,5-triene showed considerable disorganization of its
architecture that could be restored back to normal on addition of black tea or free
catechins. The tea extract in comparison to free catechin seemed to be a better
protecting agent against various types of oxidative stressCS013. Ethanol/water (7:3)
extract of green tea, tested on 2,2-azino-di- 3-ethylbenzthiazoline sulphonate,
produced antioxidant activity compared with that of ascorbic acid (10 mmol/L)CS018. The Nonpolyphenolic
fraction of residual green tea (after hot water extraction) produced a significant
suppression against hydroperoxide generation from oxidized linoleic acid in a
dose-dependent manner. Using silica gel TLC plate, chlorophylls a and b,
pheophytins a and b, -carotene, and lutein were isolated. All of
these constituents exhibited significant antioxidant activites, the ranks of
suppressive activity against hydroperoxide generation were chlorophyll a >
lutein> pheophytin a > chlorophyll b > b-carotene> pheophytin bCS047.
Antiproliferative
activity. Green tea fractions, tested on human stomach cancer (MK-1)
cells, indicated six active flavan-3-ols, epicatechin, epigallocatechin,
epigallocatechin gallate, gallocatechin, epicatechin gallate, and gallocatechin
gallate. Among the six active flavan-3-ols, epigallocatechin gallate and
gallocatechin gallate produced the highest activity. Epigallocatechin, gallocatechin,
and epicatechin gallate followed next, and the activity of epicatechin was
lowest. This suggests that the presence of the three adjacent hydroxyl groups (pyrogallol
or galloyl group) in the molecule would be a key factor for enhancing the activityCS032.
Antiprotozoan
activity. Ethanol (50%) extract of the entire plant, in broth culture at a
concentration of 125 g/mL, was inactive on Entamoeba histolyticaCS161.
Antispasmodic
activity. Hot water extract and tannin fraction of the dried entire plant were
active on the rabbit and rat intestines vs pilocarpine-induced spasms and
bariuminduced contractionsCS160.
Antiviral activity.
Epigallocatechin-3-gallate,
administered to Hep2 cells in culture, produced a therapeutic index of 22 and
an IC50 of 25 M. The agent was the most effective when
added to the cells during the transition from the early to the late phase of viral
infection suggesting that the polyphenol inhibits one or more late steps in
virus infectionCS016. Ethanol (50%) extract of the entire plant, in broth culture at
a concentration of 50 g/ mL, was inactive on Raniket and Vaccinia virusesCS161. Hot water extract
of the leaf in cell culture was active on Coxsackie A9, B1, B2, B3, B4, and B6
viruses, Echo type 9 virus, herpes simplex virus, poliovirus III, vaccinia
virus, and REO type 1 virusCS163.
Anti-yeast
activity. Ethanol (50%) extract of the entire plant, in broth culture at a
concentration of 1 mg/mL, was inactive on Candida albicans, Cryptococcus
neoformans, and Sporotrichum schenckiiCS161. Ethanol extract
of the leaf on agar plate produced MIC 9.3 mg/mL on Candida albicans CS164.
Coronary heart disease
prevention. Tea, taken by men and women age 30 to 70 years at a dose of
480.0 mL per day, produced a positive dose–response effectCS008.
Cytochrome P50
expression. Fresh leaves of green, black, and decaffeinated black tea enhanced
lauric acid hydroxylation. The decaffeinated black tea produced no significant effect.
Green tea and black tea but not decaffeinated black tea, stimulated the Odealkylations
of methoxy-, ethoxy-, and pentoxy-resorufin indicating upregulation of
cytochrome P50 (CYP)1A and CYP2B. Immunoblot analysis revealed that green and
black tea, but not decaffeinated black tea, elevated the hepatic CYP1A2
apoprotein levels. Hepatic microsomes from green and black tea-treated rats,
but not those from the decaffeinated black tea-treated rats, were more
effective than controls in converting IQ into mutagenic species in the Ames
testCS001.
Dental enamel
erosion. Herbal tea and conventional black tea, tested on teeth, resulted
in erosion of dental enamel. After exposure to tea, sequential profilometric tracings
of the specimens were taken, superimposed, and the degree of enamel loss
calculated as the area of disparity between the tracings before and after
exposure. Tooth surface loss resulted from herbal tea (mean 0.05 mm2) was significantly
greater than that which resulted from exposure to conventional black tea (0.01
mm2), and water (0.00 mm2)CS022. Tannin, catechin, caffeine, and tocopherol, tested in vitro on
tooth enamel, demonstrated that these components possess the property of
increasing the acid resistance of tooth enamel. The effects increased dramatically
when the components were used in combination with fluoride. A mixture of tannic
acid and fluoride showed the highest inhibitory effect (98%) on calcium release
to an acid solution. Tannin in combination with fluoride inhibited the
formation of artificial enamel lesions in comparison with acidulated phosphate fluoride
(APF) as determined by electron probe microanalysis, polarized-light
microscopy, and Vickers microhardness measurementCS024.
DNA effect. Green tea extract,
in cell culture at a dose of 10 mg/L corresponding to 15 mmol/L EGCg for 24
hours, did not protect Jurkat cells against H2O2-induced DNA damage.
The DNA damage, evaluated by the Comet assay, was dose-dependent. However, it
reached plateau at 75 mmol/L of H2O2 without any
protective effect exerted by the extract. The DNA repair process, completed
within 2 hours, was unaffected by supplementationCS021.
Fluoride retention.
Tea,
used as a mouth rinse, demonstrated strong avidity of enamel for tea and
salivary pellicle components. Thirty-four percent of the fluoride was retained
in the oral cavity. Differences in retention at the tooth surface in the
presence and absence of an acquired pellicle were not statistically significant
at incisor or molar sites. Fluoride from tea showed strong binding to enamel
particles, which was only partially dissociated by solutions of ionic strength
considerably greater than that of salivaCS012.
Gastrointestinal
effect. Green tea, administered to rats fasted for 3 days, reverted to normal
the mucosal and villous atrophy induced by fasting. Black tea ingestion had no
effect. Ingestion of black tea, green tea, and vitamin E before fasting
protected the intestinal mucosa against atrophyCS003. Characterization of
melanin extracted from tea leaves proved similarity of the original compound to
standard melanin. The Langmuir adsorption isotherms for gadolinium (Gd) binding
were obtained using melanin. Melanin–Gd preparation demonstrated low acute
toxicity. LD50 for the preparation was in a range of 1.25–1.50 g/kg in mice.
Magnetic resonance imaging (MRI) properties of melanin itself and melanin-Gd
complexes have been estimated. Gadoliniumfree melanin fractions possess
slighter relaxivity compared with its complexes. The relaxivity of lower
molecular weight fraction was 2 times higher than relaxivity of Gd(DTPA)
standard. Postcontrast images demonstrated that oral administration of melanin
complexes in concentration of 0.1 mM provides essential enhancement to longitudinal
relaxation times (T[1])-weighted spin echo image. The required contrast and
delineation of the stomach wall demonstrated uniform enhancement of MRI with
proposed melanin complexCS049.
Hypocholesterolemic
effect. Green tea, in human HepG2 cell culture, increased both LDL
receptor-binding activity and protein. The ethyl acetate extract, containing 70%
(w/w) catechins, also increased LDL receptor-binding activity, protein, and mRNA,
indicating that the effect was at the receptor level of gene transcription and
that the catechins were the active constituents. The mechanism by which green
tea upregulated the LDL receptor was investigated. Green tea decreased the cell
cholesterol concentration (–30%) and increased the conversion of the
sterol-regulated element binding protein (SREBP-1) from the inactive precursor
form to the active transcription-factor form. Consistent with this, the mRNA of
3-hydroxy-3-methylglutaryl coenzyme-A reductase, the rate limiting enzyme in cholesterol
synthesis, was also increased by green teaCS050.
Immunomodulatory
effect. To determine the effects of tea on transplant-related immune
function in vitro lymphocyte proliferation tests using phytohemagglutinin, mixed
lymphocytes culture assay, IL-2, and IL-10 production from mixed lymphocyte proliferation
were performed. Tea had immunosuppressive effects and decreased alloresponsiveness
in the culture. The immunosuppressive effect of tea was mediated through a
decrease in IL-2 productionCS038. Tea, assayed in cell culture, enhanced
neopterin production in unstimulated peripheral mononuclear cells, whereas an
effective reduction of neopterin formation in cells stimulated with
concanavalin A, phytohemagglutinin or interferon (IFN)- was observedCS041. Theaflavins potently
suppressed IL-2 secretion, IL-2 gene expression, and the activation of NF-B
in murine spleens enriched for CD4(+) T-cells. Theaflavins also inhibited the
induction of IFN- mRNA. However, the expression of the T(H2)
cytokines IL-4 and IL-5, which lack functional NF-B sites within their
promoters was unexpectedly suppressed by theaflavins as wellCS046.
Insulin-enhancing
effect. Tea, as normally consumed, was shown to increase insulin activity
more than 15-fold in vitro in an epididymal fat cell assay. The majority of the
insulin-potentiating activity for green and oolong teas was owing to
epigallocatechin gallate. For black tea, the activity was present in addition
to epigallocatechin gallate, tannins, theaflavins, and other undefined compounds.
Several known compounds found in tea were shown to enhance insulin with the
greatest activity due to epigallocatechin gallate followed by epicatechin gallate,
tannins, and theaflavins. Caffeine, catechin, and epicatechin displayed insignificant
insulin-enhancing activities. Addition of lemon to the tea did not affect the
insulin-potentiating activity. Addition of 5 g of 2% milk per cup decreased the
insulin-potentiating activity one-third, and addition of 50 g of milk per cup
decreased the insulin-potentiating activity approx 90%. Non-dairy creamers and
soymilk also decreased the insulinpotentiating activityCS034.
Iron absorption. Tea, administered
by gastric intubation to rats, did not affect iron absorption when tea was
consumed for 3 days but when delivered in tea the absorption was decreased.
Rats maintained on a commercial diet were fasted overnight with free access to
water and then gavaged with 1 mL of 59Fe labeled FeCl3
(0.1 mM or 1 mM) and lactulose (0.5 M) in water or black
tea. Iron absorption was estimated from Fe retention. Intestinal permeability
was evaluated by lactulose excretion in the urine. Iron absorption was lower
with given with tea at both iron concentrations but tea did not affect
lactulose excretionCS004.
Lipid peroxidation
activity. Solubilized green tea, administered orally to rats for 5 weeks,
reduced lipid peroxidation products. The treatment produced increased activity of
glutathione (GSH) peroxidase and GSH reductase, increased content of reduced GSH,
a marked decrease in lipid hydroperoxides and malondialdehyde in the liver, an increase
in the concentration of vitamin A by about 40%. A minor change in the measured parameters
was observed in the blood serum. GSH content increased slightly, whereas the
index of the total antioxidant status increased significantly. In contrast, the
lipid peroxidation products, particularly malondialdehyde, was significantly
diminished. In the central nervous tissue, the activity of superoxide dismutase
and glutathione peroxidase decreased, whereas the activity of GSH reductase and
catalase increased after drinking green tea. Moreover, the level of lipid
hydroperoxides, 4-hydroksynonenal, and malondialdehyde decreased significantlyCS036.
Neuromuscular-blocking
action. Thearubigin fraction of black tea was investigated for
neuromuscular-blocking action of botulinum neurotoxin types A, B, and E in the mouse
phrenic nerve-diaphragm preparations. On binding, A (1.5 nM), B (6 nM),
and E (5 nM) abolished indirect twitches within 50, 90, and 90 minutes,
respectively. Thearubigin fraction mixed with each toxin protected against the
neuromuscular-blocking action of botulinum neurotoxin types A, B, and E by
binding with the toxinsCS037.
Oral submucousal
fibrosis effect. Tea, administered orally to 39 patients with oral submucous fibrosis,
indicated that the treatment was effective for patients with abnormal
hemorheology. The patients were divided into control and experimental groups.
The control group included 22 oral submucous fibrosis patients who were treated
by oral administration of vitamins A and D, vitamin B complex, and vitamin E. The
experimental group included 17 patients who were treated with vitamins and tea
pigment after their examination of hemorheology. The results showed that 7 of 12
patients in the experimental group with abnormal hemorheology had average 7.9 mm
improvement on the open degree (58.3%), and the open degree of the other five patients
whose hemorheology was normal only increased 2 mm (20%). The therapeutical
results of the experimental group (58.3%) were significantly better than that
of the control group (13.6%) (p <0.005)CS035.
P-glycoprotein
activity. Green tea polyphenols (30 g/mL) inhibited the
photolabeling of P-gp by 75% and increased the accumulation of rhodamine-123
threefold in a multidrug-resistant cell line CH(R)C5, indicating that the
polyphenols interact with P-gp and inhibit its transport activity. The modulation
of P-gp transport by polyphenols was a reversible processCS045.
Photoprotection
effect. Tea extracts, administered topically, produced a dosedependent
inhibition of the erythema response evoked by UV radiation. The (–)-epigallocatechin-3-gallate
and (–)-epicatechin-3-gallate polyphenolic fractions were most efficient at
inhibiting erythema, whereas (–)-epigallocatechin and (–)-epicatechin had
little effect. On histological examination, skin treated with the extracts
reduced the number of sunburn cells and protected epidermal Langerhans cells from
UV damage. The extract also reduced damage that formed after UV radiationCS006. Green tea
polyphenols, applied topically to the human skin, prevented UVB-induced
cyclobutane pyrimidine dimers, which are considered to be mediators of
UVB-induced immune suppression and skin cancer induction. The treatment, prior
to exposure to UVB, protected against UVB-induced local as well as systemic
immune suppression in laboratory animals. Additionally, treatment of mouse skin
inhibited UVB-induced infiltration of CD11b cells. CD11b is a cell-surface marker
for activated macrophages and neutrophils, which are associated with induction of
UVB-induced suppression of contact hypersensitivity responses. The treatment also
resulted in reduction of the UVBinduced immunoregulatory cytokine IL-10 in skin
as well as in draining lymph nodes, and an elevated amount of IL-12 in draining
lymph nodesCS026.
Protease
inhibition. Epigallocatechin-3- gallate, in cell culture at a concentration
of 100 M, reduced virus yield by 2 orders of magnitude
producing an IC50 of 25 M and a therapeutic index of 22 in Hep2
cells. The agent was the most effective when added to the cells during the
transition from the early to the late phase of viral infection, suggesting that
it inhibited one or more late steps in virus infection. One of these steps
appears to be virus assembly, because the titer of infectious virus and the
production of physical particles were much more affected than the synthesis of
virus proteins. Another step might be the maturation cleavages carried out by adenain.
When tested on adenain, epigallocatechin-3-gallate produced an IC50 of 109 MCS017.
Radical scavenging
activity. Green tea, evaluated using the 1,1-diphenyl-2-picrylhydrazyl radical,
indicated that the galloyl moiety showed more potent activity. The contribution
of the pyrogallol moiety in the B-ring to the scavenging activity seemed to be
less than that of the galloyl moietyCS032.
Tetanus toxin
protection. Thearubigin fraction of black tea was investigated for neuromuscular-blocking
action on tetanus toxin in the mouse phrenic nerve-diaphragm preparations and
on binding of this toxin to the synaptosomal membrane preparations of rat
cerebral cortices. Tetanus toxin (4 g/mL) abolished indirect twitches
in the mouse phrenic nerve–diaphragm preparations within 150 minutes.
Thearubigin fraction mixed with tetanus toxin blocked the inhibitory effect of
the toxinCS030.
Toxicity. Green tea,
administered orally at a dose of 6 g per day in six doses to 42 patients who
were asymptomatic and had manifested, progressive prostate specific antigen
elevation with hormone therapy, produced grade 1 or 2 toxicity in 69% of the patients
and included nausea, emesis, insomia, fatigue, diarrhea, abdominal pain, and
confusion. However, six episodes of grade 3 toxicity and one episode of grade 4
toxicity also occurred, with the latter manifesting as severe confusionCS031.
Toxicity assessment. Ethanol (50%) extract
of the entire plant, administered intraperitoneally to mice produced lethal dose
(LD)50 316 mg/kgCS161. Ethanol (95%) extract of the leaf, administered by gastric intubation
to mice, produced LD50 10 g/kg. Intraperitoneal administration produced CD90 0.7 g/kgCS166.
INDICATIONS (GREEN OR BLACK TEA)
(Duke, J. A et al., 2002)
Acute Diarrhea (1; SHT); ADD (f; DAA); Agitation (f; PH2);
Alcoholism (f; PH2); Allergy (1; WO2); Alzheimer’s (1; COX; FNF); Ameba (1;
APA); Angina (1; DAA); Anorexia (f; PH2); Apoplexy (f; JNU); Arthrosis (1; COX;
FNF); Asthma (1; AKT; APA; WO2); Atherosclerosis (1; APA; JNU; WO2); Bacteria
(1; AKT; APA; WO2); Bite (f; DAA); Bladder Stone (f; WO2); Bleeding (1; APA;
WO2); Bronchosis (1; WO2); Bruise (f; DAA); Burn (f; DAA); Cancer (1; APA; COX;
FNF); Cancer, breast (1; PH2); Cancer, colon (1; APA; PH2); Cancer, esophagus
(1; APA; JNU; WO2); Cancer, intestine (1; PH2; WO2); Cancer, liver (1; APA);
Cancer, lung (1; APA; PH2; WO2); Cancer, pancreas (2; PH2; APA); Cancer, rectum
(2; PH2); Cancer, skin (1; JNU; APA); Cancer, stomach (2; JNU; PH2; WO2);
Capillary Fragility (1; PH2); Cardiopathy (1; APA; PH2; SKY); Caries (2; AKT; JAD;
PH2); Circulosis (f; PH2); Cold (1; APA; JNU; WO2); Colic (f; JNU); Colitis (1;
APA); Congestion (1; APA); Cough (1; APA); Cramp (1; AKT); Cystosis (f; WO2);
Depression (1; PH2); Diarrhea (1; AKT; APA; PHR); Diabetes (1; APA); Dropsy (f;
DAA); Dysentery (1; PNC; WO2); Dyspepsia (f; PH2); Edema (f; DAA; WO2); Emphysema
(1; DAA); Encephalosis (f; WO2); Enterosis (1; APA; PH2); Enterovirus (1; WO2);
Epilepsy (f; DAA; JNU); Escherichia (1; PH2); Esophagosis (1; APA); Fatigue (f;
DAA; PH2); Fever (f; PH2; WO2); Gastrosis (f; PHR; PH2); Gingivosis (1; SKY);
Goiter (1; WO2); Gout (f; WO2); Hangover (f; DAA); Headache (1; APA; PH2);
Hepatosis (f; PH2; WO2); Herpes (1; AKT); High Blood Pressure (f; SKY); High
Cholesterol (1; AKT; APA; SKY; WO2); High Triglyceride (1; SKY); Hyperdipsia (f;
PH2); Hyperthyroidism (1; WO2); Immunodepression (1; AKT; FNF; SKY); Infection (1;
SKY); Inflammation (1; APA; COX; FNF; PH2); Kidney Stone (f; WO2); Lethargy (1;
JNU); Leukemia (1; WO2); Malaria (f; PH2); Melanoma (f; JNU); Metastasis (f;
JNU); Migraine (f; DAA; JNU; PH2); Nausea (f; PHR; PH2); Nephrosis (f; WO2);
Obesity (1; APA; FNF; JNU); Odontorrhagia (1; APA); Ophthalmia (f; DAA); Pain
(1; JAD; PH2); Paralysis (f; JNU); Plaque (2; PH2); Polyp (1; APA); Shingle (1;
AKT); Smallpox (f; DAA); Stone (f; JNU); Streptococcus (1; PH2); Stroke (1;
APA; JNU); Sunburn (1; APA); Swelling (f; DAA); Toxemia (f; DAA); Tuberculosis
(f; JNU); Ulcer (1; AKT; APA); Vertigo (f; JNU); Virus (1; AKT; FNF; WO2);
Vomiting (f; PH2); Water Retention (1; APA; PH2); Wrinkle (1; APA).
(Not covered by
Commission E (KOM)).
PRODUCT
AVAILABILITY (Barnes, J et al., 2007)
Tablets, capsules, dried/liquid extract, tea
PLANT PART USED
(Barnes,
J et al., 2007)
Dried leaves
DOSAGES (Barnes, J
et al., 2007)
Green
tea is standardized to 60% polyphenols.
v Adult PO extract:
250-400 mg/day of standardized to 90% polyphenols (McCaleb et al, 2000)
v Adult
PO tea: 1 tsp tea leaves in 8 oz hot water, drink 2-5 cups/day (McCaleb et al,
2000)
DOSAGES
(GREEN Or BLACK Tea) (Duke, J. A et al.,
2002)
v 1–2 tsp dry
leaf/cup water 1–3 ×/day (APA)
v 50–100 mg green tea
polyphenols (APA);
v 100–200 mg StX (50%
polyphenols) (APA);
v three 333-mg green
tea capsules, each containing 50 mg polyphenols/day (APA).
PREPARATION TIPS (Dole Food Company, Inc. 2002)
The best tea is made using whole or large fragments of tea leaves,
available in many specialty tea shops. Many of these shops also sell implements,
such as mesh containers, which allow tea leaves to infuse their flavor into
water without leaving the leaves behind. To make a good cup or pot of tea,
start by using cold, fresh, and filtered water (if you don’t like the taste of your
tap water).
Heat
the water to a simmer—do not boil—remove from heat, and add the tea. Steeping guidelines
are generally 1 teaspoon of tea per cup of water, but the amount may vary according
to the type of tea used. Green teas usually need to be steeped in water for 1
to 2 minutes, and black teas may require 3 to 4 minutes. Avoid oversteeping.
More than 5 minutes can make all types of tea bitter.
TEAS AND POSSIBLE HEALTH (Dole Food Company, Inc. 2002)
BENEFITS
Tea
has been consumed throughout history for its supposed curative powers, and medical research now suggests that there are health benefits from drinking green and
black teas.
Several studies show an association between consumption of green
tea and reduction in the risk for cancer and heart disease. Green tea naturally
contains chemical compounds called polyphenols. Within this family of compounds
are chemicals that appear to play a role in cell growth and programmed cell
death, which could be important in preventing and controlling cancer. Polyphenols
also are antioxidants that can help prevent cell damage and may help prevent formation
of plaque in the arteries.
SERVING SUGGESTIONS (Dole Food Company, Inc. 2002)
Tea is an excellent beverage at any time of the day. Black teas
are typically served at breakfast, often with milk and sweeteners. Herbal teas
typically do not contain the stimulant caffeine and thus are excellent choices
in the evening. One note of caution: tea itself contains no calories. However, lighteners
or sweeteners added to it can add a
significant amount of calories and fat. Minimize fat and calories by using skim
milk. In addition, afternoon tea, an old but widespread tradition, often
includes baked sweets such as scones or cookies.
Keep
your tea break healthful by limiting these sweets. Serve fruit or slices of
wholegrain bread instead.
CONTRAINDICATIONS,
INTERACTIONS, AND SIDE EFFECTS (GREEN or BLACK TEA)
(Duke,
J. A et al., 2002)
Class
2D
Fermented black tea not recommended for excess or long-term use
(AHP). In excess can cause GI distress and nervous irritability (due to
caffeine) (PNC). Caffeine syndrome in overindulgence, as with coffee, etc.
(SKY). All things in moderation. One woman who consumed the equivalent of 65 g
tea leaves/day for 5 years exhibited liver dysfunction. Ascites and
splenomegaly resolved after tea was discontinued (SHT). Pedersen, who does not
cover conventional tea, says that peppermint leaf contains much astringent tannin,
which can damage the liver and intestine with prolonged use (Pedersen, 1998).
Since the more widely used tea (Camellia sinensis) often contains twice
as much tannin as peppermint, this recommendation should be doubly pertinent
under tea, or maybe we should call these tannins by the more attractive names “OPCs,
polyphenols, and pycnogenols” and declare them useful antioxidant good guys
instead of hepatotoxic bad guys (JAD). Regarding caffeine, “Pregnant women
should under no circumstances exceed a dosage of 300 mg/day (5 cups of tea spread
out over the course of a day). Infants whose nursing mothers consume beverage
containing caffeine could suffer from sleep disorders” (APA).
CONTRAINDICATIONS (Barnes, J et al., 2007)
Green tea should not be used by persons with
hypersensitivity to this product or by those with kidney infl ammation,
gastrointestinal ulcers, insomnia, cardiovascular disease, or increased
intraocular pressure. This herb contains caffeine. Decaffeinated tea is
available, although some caffeine may remain.
SIDE EFFECTS/ADVERSE REACTIONS (Barnes, J et al., 2007)
v CNS:
Anxiety, nervousness,
insomnia (high doses)
v CV:
Increased blood
pressure, palpitations, irregular heartbeat (high doses)
v GI:
Nausea, heartburn,
increased stomach acid (high doses)
v INTEG:
Hypersensitivity
reactions
INTERACTIONS (Barnes, J et al., 2007)
Drug
v Antacids:
Antacids may decrease
the therapeutic effects of green tea (theoretical).
v Anticoagulants,
antiplatelets: Green
tea with anticoagulants, antiplatelets may increase risk of bleeding (theoretical)
(Jellin et al, 2008).
v Beta-adrenergic
blockers: Green
tea used with these agents can lead to increased inotropic effects.
v Benzodiazepines:
Green tea with these
agents increases sedation (theoretical) (Jellin et al, 2008).
v Bronchodilators,
xanthines (theophylline): Large amounts of green tea increase the action
of xanthines, some bronchodilators.
v MAOIs
(isocarboxazid, phenelzine, tranylcypromine):
Green tea used in
large amounts taken with MAOIs can lead to hypertensive crisis, do not use together.
INTERACTIONS—CONT’D (Barnes, J et al., 2007)
Herb
Ephedra:
Concurrent use of
ephedra and caffeinated green tea may increase hypertension and CNS
stimulation; avoid concurrent use with caffeinated green tea products.
Food
Dairy
products: Dairy
products may decrease the therapeutic effects of green tea.
Iron:
Green tea may decrease
iron absorption.
Lab
Test
Glucose,
VMA, urine creatine, urine catecholamine: Green tea may increase these levels.
CLIENT CONSIDERATIONS (Barnes, J et al., 2007)
Assess
v Assess the reason the client is using green
tea.
v Assess for hypersensitivity reactions. If
present, discontinue the use of this herb and administer an antihistamine or
other appropriate therapy.
v Assess for other conditions that are
contraindications to green tea use, including cardiovascular and renal disease,
and increased intraocular pressure.
v Assess for use of antacids, dairy products,
and ephedra (see Interactions).
Administer
v Instruct the client to store green tea in a
cool, dry place, protected from heat and moisture.
Teach
Client/Family
v Caution the client with renal or
cardiovascular disease, or increased intraocular pressure not to use green tea
products that contain caffeine.
v Teach the client not to use green tea with
antacids or milk because its effect is decreased.
EXTRACTS (GREEN OR BLACK TEA) (Duke, J. A et al., 2002)
Both the polphenols (OPCs, tannins) and
xanthines (caffeine) have their good and bad sides. As a major source of
the major COX-2 Inhibitor ([+]-catechin), this might be viewed by
enthusiasts as another herbal miracle aspirin (COX). See FNF. Muroi and
Kubo (1993) demonstrated synergies for antibacterial activity in compounds from
tea (Camellia sinensis), “... green tea extract is
effective in the prevention of dental caries because of the antibacterial
activity of flavor compounds together with the antiplaque activity of
polyphenols.... Synergism was found in the combination of sesquiterpene
hydrocarbons (delta-cadinene and beta-caryophyllene) with indole; their
bactericidal activities increased from 128-fold to 256- fold ... the
combination of 25 μg/mL delta-cadinene and 400 μg/mL indole reduced the number
of viable (bacterial) cells at any stage of growth.” Translation: The
mixture (“herbal shotgun”) of three bactericidal compounds that might
help prevent plaque was more than 100 times more potent than the
isolated individual compounds (“magic bullet”). And then there is the natural fluoride
(130–160 ppm) (PDR).
REFERENCE
Barnes,
J., Anderson, L. A., and Phillipson, J. D. 2007. Herbal Medicines
Third Edition. Pharmaceutical Press. Auckland and London.
Dole Food Company, Inc. 2002. Encyclopedia of Foods A Guide to
Healthy Nutrition. Academic Press. San Diego, California.
Duke,
J. A. with Mary Jo Bogenschutz-Godwin, Judi duCellier, Peggy-Ann K. Duke. 2003. Handbook of
Medicinal Spices. CRC Press LLC. USA.
Ross,
I. A. 2005. Medicinal
Plants of the World Vol. 3. Chemical Constituents, Traditional and Modern
Medical Uses. Human Press. Totowa, New Jersey.
No comments:
Post a Comment