CAMELLIA SINENSIS 1

1 Camellia
sinensis
L.

Common Names
Aisiksikimi United States Te Denmark
Caj Albania Te Faroe Islands
Caj Croatia Te France
Caj Czech Republic Te Italy
Caj Hawaii Te Norway
Caj Serbia Te Spain
Cay Turkey Te Surinam
Ceai Romania Te Switzerland
Cha Brazil Te Wales
Cha China Tea plant England
Cha Hawaii Tea Australia
Cha Japan Tea England
Cha Pacific Islands Tea Guyana
Cha Portugal Tea Hungary
Chai Bulgaria Tea United States
Chai Mozambique Tebusk Denmark
Chai Russia Tebuske Sweden
Chai Tanzania Tee Finland
Chai Ukraine Tee Germany
Chai Zaire Tee Netherlands
Chaj Macedonia Tee South Africa
Chayna roslina Ukraine Teepensas Finland
Chinesischer tea Germany Tey The Isle of Man (Manx)
Cunuc yacu Ecuador Teye Northern Sotho
Eaj Czech Republic The France
Eajovnik Czech Republic The Indonesia
Herbata Poland The Malaysia
Icayi Rwanda Thee Netherlands
Ilitye Africa Theesoort Netherlands
Itiye Africa Theestrauch Germany
Oti United States Theestruik Netherlands
Taa Germany Theler France
Tae Ireland Ti Congo
Te Cornwall Ti Samoa

From: Medicinal Plants of the World, vol. 3: Chemical Constituents, Traditional and Modern Medicinal Uses
By: I. A. Ross © Humana Press Inc., Totowa, NJ

1
2 MEDICINAL PLANTS OF THE WORLD

Ti Scotland Tra Vietnam

Tii Greenland Tsa Philippines
Tii New Zealand Yaku-q’oniwan Ecuador
Tii Northwest Territories, Canada Zaya Turkmenistan

BOTANICAL DESCRIPTION TRADITIONAL MEDICINAL USES

Camellia sinensis is an evergreen tree or India. Decoctions of the dried and fresh
shrub of the THEACEAE family that grows buds and leaves are taken orally for head-
to 10–15 m high in the wild, and 0.6–1.5 m ache and feverCS145. Powder or decoction of
under cultivation. The leaves are short- the dried leaf is applied to teeth to prevent
stalked, light green, coriaceous, alternate, tooth decayCS146. Fresh leaf juice is taken
elliptic-obovate or lanceolate, with serrate orally for abortionCS155, and as a contracep-
margin, glabrous, or sometimes pubescent tive and hemostaticCS147.
beneath, varying in length from 5 to 30 cm, Mexico. Hot water extract of the leaf is
and about 4 cm wide. Young leaves are pu- taken orally by nursing mothers to increase
bescent. Mature leaves are bright green in milk productionCS148.
color, leathery, and smooth. Flowers are Turkey. Leaves are taken orally to treat
white, fragrant, 2.5–4 cm in diameter, soli- diarrheaCS149.
tary or in clusters of two to four. They have China. Hot water extract of the dried leaf is
numerous stamens with yellow anthers and taken orally as a sedative, an antihyperten-
produces brownish-red, one- to four-lobed sive, and anti-inflammatoryCS108.
capsules. Each lobe contains one to three Guatemala. Hot water extract of the dried
spherical or flattened brown seeds. There leaf is used as eyewash for conjunctivitisCS154.
are numerous varieties and races of tea. Kenya. Water extract of the dried leaf is
There are three main groups of the cultivated applied ophthalmically to treat corneal
forms: China, Assam, and hybrid tea, differ- opacities CS150. The infusion is used for
ing in form. Camellia sinensis assamica, the chalzion and conjunctivitisCS151.
source of much of the commercial tea crop Thailand. Hot water extract of the dried leaf
of Ceylon is a tree that, unpruned, may attain is taken orally as a cardiotonic and
a height of 15 m and has proportionally neurotonicCS152. Hot water extract of the
longer, thinner leaves than typical species. dried seed is taken orally as an anti-
ORIGIN AND DISTRIBUTION fungalCS153.
The cultivation and enjoyment of tea are CHEMICAL CONSTITUENTS
recorded in Chinese literature of 2700 BC (ppm unless otherwise indicated)
and in Japan about 1100. Through the Acetaldehyde, phenyl: Sh 1.52–1.78%CS100
Arabs, tea reached Europe about 1550. Acetaldehyde: LfCS073
Native to Assam, Burma, and the Chinese Acetamide, N-ethyl: LfCS027
province of Yunnan, it is highly regarded in Acetic acid: LfCS086
southern Asia and planted in India, south- Acetoin: LfCS068
ern Russia, East Africa, Java, Ceylon, Acetone: LfCS091
Sumatra, Argentina, and Turkey. China, Acetophenone, 2-4-dimethyl: LfCS027
India, Indonesia, and Japan produced about Acetophenone, 3-4-dimethoxy: LfCS027
a half of the total world production. Acetophenone, para-ethyl: LfCS027
CAMELLIA SINENSIS 3

Acetophenone: Headspace volatileCS044 Benzene, 1-2-5-trihydroxy: LfCS003

Actinidiolide, dihydro: Lf EOCS132 Benzene, 1-2-dimethoxy: LfCS077
Afzelechin, epi, (–): Lf 350CS084 Benzene, 1-2-dimethoxy-4-ethyl: LfCS077
Afzelechin, epi, 3-O-gallate (–): Lf 37CS005 Benzene, 1-2-dimethoxy-4-methyl: LfCS077
Afzelechin, epi, 3-O-gallate (4-b-6)-epi, Benzene, 1-3-diacetyl: LfCS027
gallocatechin-3-O-gallate: Lf 5.6CS008 Benzene, 1-4-diacetyl: LfCS027
Allantoic acid: PlCS033 Benzoic acid: Headspace volatileCS044
Allantoin: PlCS033 Benzothiazole, 2-methyl: LfCS036
Aluminium inorganic: LfCS028 Benzothiazole: LfCS036
Amyrin, D: Sd oilCS095 Benzoxazole: LfCS036
Amyrin, E: Sd oil 76CS095 Benzyl alcohol: Lf EO 1.01–1.6%CS136,
Aniline, N-ethyl: LfCS027 Headspace volatileCS044, LfCS091,
Aniline, N-methyl: LfCS027 Sh 0.09–0.14%CS100
Aniline: LfCS027 Benzyl butyrate: LfCS002
Apigenin: LfCS108 Benzyl ethyl ketone: LfCS002
Apigenin-6-8-di-C-E-D-arabinopyranosyl: Benzylaldehyde, 2-methyl: LfCS002
Lf 20CS156 Benzylaldehyde, 4-methoxy: LfCS002
Apigenin-6-8-di-C-glucoside: ShCS096 Benzylaldehyde: Headspace volatileCS044,
Arbutin: Lf 0.2CS078 LfCS077, Sh 0.21–0.23%CS100
Aromadenrin: ShCS094 Benzylamine: N-N-dimethyl: LfCS027
Ascorbic acid: ShCS038, Lf 0.257%CS048 Bicyclo(4.3.0)non-8-en-7-one, 1-5-5-9-
Assamicain A: Lf 58.2CS007 tetramethyl: LfCS002
Assamicain B: Lf 76.6CS007 Brassicasterol: Sd oilCS134
Assamicain C: Lf 33.6CS007 Brassinolide, 28-homo, 6-keto: LfCS135
Assamsaponin A: Sd 0.01%CS021 Brassinolide, 28-nor, 6-keto: LfCS135
Assamsaponin B: Sd 28.3CS021 Brassinolide, 28-nor: LfCS135
Assamsaponin C: Sd 36.5CS021 Brassinolide, 6-keto: LfCS135
Assamsaponin D: Sd 26.1CS021 Brassinolide: Lf 0.0046 ppbCS089
Assamsaponin E: Sd 11.1CS021 Brassinone, 24(S)-ethyl: Lf 30 ng/65 kgCS110
Assamsaponin F: Sd 14.1CS021 Brassinone, 24-ethyl: LfCS089
Assamsaponin G: Sd 79.1CS021 Brassinone: Lf 130 ng/65 kgCS110
Assamsaponin H: Sd 13.4CS021 Butan-2-ol: LfCS068
Assamsaponin I: Sd 98.5CS021 Butyrate, ethyl-3-hydroxy: LfCS068
Astragalin: LfCS139 Butyroin: LfCS068
Avicularin: LfCS058 Butyrospermol: Sd oilCS095
Barrigenol, A-1: PlCS118 Caffeine: Lf 0.381–9.9%CS114,CS049, ShCS038, Pl,
Barringtogenol C, 3-O-E-D-galacto- Call TissCS050, SdCS093, Sd Ct, Peduncle,
pyranosyl(1-2) E-D-xylopyranosyl PcCS102, Fl bud, Stamen, Pistil, FlCS107, An
(1-2)D-l-arabinopyranosyl(1-3)E-D- 0.05–6.77 ppt, Stem call 0.64 pptCS099,
glucuronopyranosyl-21-O-cinnamoyl- PetalCS117, FrCS037
16-22-di-O-acetyl: LfCS013 Camellia galactoglucan: LfCS067
Benzene, 1-2-3-trimethoxy: LfCS077 Camellia polysaccharide: LfCS122
Benzene, 1-2-3-trimethoxy-5-ethyl: LfCS077 Camellia saponin B, deacyl: LfCS081
Benzene, 1-2-3-trimethoxy-5-methyl: LfCS077 Camellia sinensis polysaccharide TSA: LfCS012
Benzene, 1-2-4-trihydroxy: LfCS003 Camellianin A: LfCS108
4 MEDICINAL PLANTS OF THE WORLD

Camellianin B: LfCS108 Catechin-3-O-gallate, epi(–): Lf 0.0086–

Camelliaside A: Sd 656–2733.3CS011,CS119 6.6%CS053,CS049
Camelliaside B: Sd 291–3026.6 CS011,CS119 Catechin-gallate, (+): LfCS082
Camelliaside C: Sd 2.5CS011 Catechin-gallate: LfCS042
Campesterol: Sd oilCS134 Catechol, (+): PlCS138
Carvacrol: LfCS002 Catechol, epi(–): ShCS128, PlCS138
Castasterone: Lf 7.2 mg/65 kgCS110 Catechol, epi, gallate(–): ShCS128
Catechin-(4-D-8)-epi-gallocatechin: Catechol, epi-gallo(–): ShCS128
Lf 45.4CS008 Catechol, epi-gallo, gallate(–): ShCS128
Catechin-(4-D-8)-epi-gallocatechin-3- Catechol, gallo, (+): ShCS128
gallate: Lf 45.4CS008 Chasaponin: PlCS035
Catechin-(4-E-8)-epi-gallocatechin-3- Chlorogenic acid: Call TissCS087, LfCS139
gallate, epi: Lf 20.8CS008 Chondrillasterol: Sd oilCS130
Catechin, (+): Lf 0.0017–2.9%CS053,CS049, Citric acid: LfCS086
Call TissCS060. St callCS099, ShCS038, Cresol, meta: LfCS003
An, StCS099 Cresol, ortho: LfCS003
Catechin, epi (–): Lf 0.004–6.8%CS053,CS049, Cresol, para: LfCS003
Call TissCS060, ShCS038, St call 0.07 pptCS099 Cyclocitral, E: Sh 0.08–0.1%CS100, LfCS002
Catechin, epi, 3-O-para-hydroxy-benzoate Cyclohex-2-en-1-4-dione, 2-6-6-trimethyl:
(–): Lf 3.6CS005 LfCS002
Catechin, epi, epi-gallo-catechin(4-E-8)- Cyclohex-2-en-1-one, 2-6-6-trimethyl:
3-O-galloyl: Lf 50CS092 LfCS002
Catechin, epi-gallo (–), 3-O-para- Damascenone, E: LfCS002
coumaroate: Lf 83.3CS140 Damascone, D: LfCS002
Catechin, epi-gallo (–): Lf 3269CS140 Damascone, E: LfCS002
Catechin, epi-gallo, 3-3'-di-O-gallate(–): Dammaridienol: Sd oil 30CS095
LfCS140 Deca-trans-2-cis-4-dien-1-al: LfCS002
Deca-trans-2-en-1-al: LfCS002
Catechin, epi-gallo, 3-4'-di-O-gallate(–):
Dehydrogenase, NADP-dependent-alco-
LfCS140
hol: SdCS031
Catechin, epi-gallo, 3-O-gallate (–):
Demmarenol, 24-methylene: Sd oilCS095
Lf 0.8718%CS140
Diphenylamine: Lf 0.013–1.17%CS098
Catechin, epi-gallo, gallate(–): St call 0.02
Dodeca-trans-2-trans-6-10-trien-1-al,
pptCS099, LfCS109
4-ethyl-7-11-dimethyl: LfCS002
Catechin, epi-gallo: LfCS140
Erucid acid: Sd oil LfCS134
Catechin-3-O-(3'-O-methyl)-gallate,
Ethyl acetate: LfCS091
epi(–): Lf 0.08%CS010
Ethyl lactate: LfCS068
Catechin-3-O-(3-O-methyl)-gallate,
Eugenol: Fr EOCS030
epi(–): Lf 70.6-96.2CS005,CS140 Euphol: Sd oilCS095
Catechin-3-O-(4-O-methyl)-gallate, Farnesene, D, trans-trans: Lf EOCS115
epi(–): Lf 16CS005 Farnesol: LfCS091
Catechin-3-O-gallate-(4-E-6)-epi- Fluoride inorganic: Lf 188CS143
gallocatechin-3-O-gallate, epi: Fluorine, inorganic: LfCS043
Lf 5.8CS008 Furan, 2-acetyl: LfCS002
Catechin-3- O-gallate-(4-E-8)-epi- Furan-3-one, tetrahydro, 2-methyl: LfCS068
gallocatechin-3-O-gallate, epi: Lf 3.6CS008 Furocoumarin, angular, 4-hydroxy-2'-
Catechin-3-O-gallate, (+): Lf 0.011%CS084 methoxy: LfCS014
CAMELLIA SINENSIS 5

Gadoleic acid: Sd oilCS134 Galloyl-E-D-glucose, 1-4-6-tri-O:

Gallic acid: LfCS051 Lf 0.01%CS010
Gallocatechin gallate, (–): Lf 0.188%CS112 Galloylcatechin, epi (–): LfCS054
Gallocatechin gallate, (+): LfCS082 Geranic acid, trans: LfCS002
Gallocatechin gallate, epi(–): LfCS125 Geraniol E-D-glucopyranoside: ShCS113
Gallocatechin gallate, epi(+): LfCS123 Geraniol: ShCS113, Lf EO 3.16-25.46%CS136,
Gallocatechin-(4-D-8)-epi-catechin: LfCS109
Lf 36.6CS008 Geranyl-E-primeveroside, 8-hydroxy:
Gallocatechin, (–): LfCS056 Lf 2.08CS018
Gallocatechin, (+): Lf 0.01–12.8%CS053,CS049 Germanicol: Sd oil 25CS095
Gallocatechin, epi(+): Lf 1.1%CS083 Germanicum inorganic: LfCS120
Gallocatechin, epi, (–): Lf 0.088- Gibberellin A-1: EndospermCS004
16.8%CS005,CS049, ShCS038 Gibberellin A-19: EndospermCS004
Gallocatechin, epi, (4-E-8)-epi-catechin- Gibberellin A-20: EndospermCS004
3-)-gallate: Lf 27.6CS008 Gibberellin A-3, iso: EndospermCS004
Gallocatechin, epi, 3-O-cinnamate(–): Gibberellin A-3: EndospermCS004
Lf 13.2CS005 Gibberellin A-38: EndospermCS004
Gallocatechin, epi, 3-3'-di-O-gallate(–): Gibberellin A-44: EndospermCS004
Lf 9CS005 Gibberellin A-8: EndospermCS004
Gallocatechin, epi, 3-4'-di-O-gallate(–): Gibberellin A-S: EndospermCS004
Lf 9CS005 Glucogallin, E: Lf 28.4CS008
Gallocatechin, epi, 3-O-gallate(–): Glucose, E-D, 1-0-galloyl-4-6-(–)-
Lf 0.714%CS005 hexahyroxy-diphenoyl: Lf 30CS092
Gallocatechin, epi, 3-O-gallate-(4-E-6)- Glucose, E-D, 1-4-6-tri-O-galloyl: Lf 5CS092
epi-catechin-3-O-gallate: Lf 4.2CS008 Glutamic acid: N-para-coumaryl: LfCS133
Gallocatechin, epi, 3-O-gallate-(4-E-8)- Heptan-1-al: Sh 0.02–0.03%CS100
epi-catechin-3-O-gallate: Lf 44CS008 Heptan-2-ol: LfCS068
Gallocatechin, epi, 3-O-para-
Heptan-2-one, 5-iso-propyl: LfCS002
coumaroate(–): Lf 38.4CS005
Heptan-2-one: LfCS002
Gallocatechin, epi, 8-C-ascorbyl-3-O-
Heptan-3-ol: LfCS068
gallate: Lf 11.2CS008
Hepta-trans-2-trans-4-dien-1-al:
Gallocatechin, epi: Lf 1.0867%CS101
Sh 0.06–0.1%CS100
Gallocatechin-3-5'-di-O-gallate, epi(–):
Hept-trans-2-en-1-al: LfCS002
Lf 0.06%CS008
Hex-1-en-3-ol: LfCS068
Gallocatechin-3-O-(3'-O-methyl)-gallate,
Hex-2-en-1-al, 5-methyl-2-phenyl: LfCS002
epi(–):Lf 38CS084
Hex-5-en-4-olide, 4-methyl: LfCS002
Gallocatechin-3-O-gallate (–): LfCS079
Hexadecane, N: LfCS091
Gallocatechin-3-O-gallate (+): LfCS157
Gallocatechin-3-O-gallate (4-E-8) epi- Hexan-1-al: ChloroplastCS129,
catechin-gallate, epi: Lf 0.06%CS010 Sh 0.55–1.03%CS100
Gallocatechin-3-O-gallate, epi(–): Hexan-1-ol, 2-ethyl: LfCS002
Lf 0.0328–21.3%CS053,CS049, ShCS038 Hexan-2-ol: LfCS068
Gallocatechin-3-O-para-coumaroate, epi Hexa-trans-2-cis-4-dien-1-al: LfCS002
(–): LfCS010 Hex-cis-3-en-1-al: Lf 370CS034
Gallocatechin-gallate, (–): LfCS042 Hex-cis-3-en-1-ol acetate: LfCS091
Gallocateuchin-3-O-gallate, epi (–): Hex-cis-3-en-1-ol butyrate: LfCS091
Lf 5.33%CS010 Hex-cis-3-en-1-ol caproate: LfCS091
6 MEDICINAL PLANTS OF THE WORLD

Hex-cis-3-en-1-ol formate: LfCS002 Kaempferol: LfCS026, ShCS094

Hex-cis-3-en-1-ol hexanoate: Kaempferol-3-O-galactosyl-rhamnosyl-
Sh 0.02–0.03%CS100 glucoside: LfCS058
Hex-cis-3-en-1-ol hex-trans-2-enoate: Kaempferol-3-O-glucosyl(1-3)rhamnosyl
LfCS002 (1-6)galactoside: LfCS009
Hex-cis-3-en-1-ol propionate: LfCS002 Kaempferol-3-O-glucosyl-rhamnoside:
Hex-cis-3-en-1-ol, E-D-glucoside: LfCS076 LfCS058
Hex-cis-3-en-1-ol: LfCS025, Lf EO 2.15– Kaempferol-3-O-glucosyl-rhamnosyl-galac-
15%CS136, Sh 0.09–0.13%CS100 toside: LfCS058
Hex-trans-2-en-1-al: LfCS065, Lf EO 1.13– Lauric acid: Sd oilCS134
25.48%CS136, Sh 2.09–3.1%CS100 Ligustrazine: LfCS027
Hex-trans-2-en-1-ol: Sh 0.04–0.06%CS100 Limonene: LfCS068
Hex-trans-2-enyl acetate: LfCS002 Linalool E-D-glucopyranoside: ShCS113
Hex-trans-2-enyl butyrate: LfCS002 Linalool oxide A: LfCS091
Hex-trans-2-enyl formate: LfCS002 Linalool oxide B: LfCS091
Hex-trans-2-enyl hexanoate: LfCS002 Linalool oxide C: LfCS091
Hex-trans-2-enyl propionate: LfCS002 Linalool oxide I: LfCS077
Hex-trans-3-enyl butyrate: LfCS002 Linalool oxide II: LfCS077
Hex-trans-3-enyl hex-cis-3-enoate: LfCS002 Linalool oxide III: LfCS077
Hex-trans-3-enyl propionate: LfCS002 Linalool oxide IV: LfCS077
Hex-trans-3-enyl-2-methyl butyrate: LfCS002 Linalool oxide: Headspace volatileCS044
Hexyl butyrate: LfCS002 Linalool, (R): LfCS074
Hexyl formate: LfCS002 Linalool, cis, oxide (furanoid): LfCS074
Hyperoside: LfCS058 Linalool, cis, oxide (pyranoid): LfCS074
Indole: LfCS109 Linalool, cis, oxide: Sh 0.06–0.16%CS100
Indole-3-methyl-ethanolate: LfCS015 Linalool, trans, oxide (furanoid): LfCS074
Inositol, myo, 2-O-E-L-arabinopyranosyl: Linalool, trans, oxide (pyranoid): LfCS074
Lf 0.4%CS116 Linalool, trans, oxide: Lf EO 3.18–
Inositol, myo, 2-O-E-L-arabinopyranoside: 4.23%CS136, Sh 0.15–0.43%CS100
Lf 0.4%CS106 Linalool: LfCS121, Headspace volatileCS044,
Inositol, myo, 2-O-E-L-arabinoside: LfCS077 ShCS113, Lf EO 8.2–19.84CS136
Ionone, D: Sh 0.03–0.05%CS100, LfCS068 Linoleic acid: Sd oilCS134, LfCS069
Ionone, E, 1'-2'-dihydro, 1'-2'-epoxy: Linolenic acid: LfCS069
Lf EOCS132 Loliolide: Lf EOCS132
Ionone, E, 1'-2'-dihydroxy, 1'-2'-threo: Lupeol: Sd oilCS062
Lf EOCS132 Malic acid: LfCS086
Ionone, E, 3'-oxo: Lf EOCS132 Malonic acid: LfCS086
Ionone, E: Lf EO 0.02–0.31%CS136, Menthol: LfCS068
Sh 0.17–0.29%CS100 Methionine, S-methyl: Lf 7–24.5 mg%CS158
Jasmonate, dihydro, methyl-trans: LfCS002 Methylamine: Lf 50CS141
Jasmone, cis: Lf EO 0.05–0.2%CS136 Morine: LfCS045
Jasmone: LfCS091 Myrcene: LfCS091
Jasmonic acid, (1R, 2R), (–): LfCS080 Myricetin: LfCS026
Jasmonic acid, (1R, 2S), (+): LfCS080 Myristic acid: Sd oilCS134, LfCS069
Jasmonic acid: PollenCS137, AnCS137, LfCS091 Naringenin: ShCS094
Kaempferitin: LfCS139 Naringenin-fructosyl-glucoside: LfCS063
CAMELLIA SINENSIS 7

Neral: LfCS002 Phenylethanol, 2: LfCS091

Nerolidol: LfCS109, Sh 0.08–0.12%CS100 Phenylethyl alcohol, 2: Sh 0.1–0.13%CS100
NH3 inorganic: Lf 400CS141 Phenylethyl alcohol: Headspace
Nicotiflorin: LfCS133 volatileCS044
Nicotine: Lf 15.5 ng/gCS047 Pheophytin A: LfCS088
Nonal-1-al: Sh 0.04–0.06%CS100 Pheophytin B: LfCS088
Nonal-2-ol: LfCS068 Pinene, a: LfCS068
Nonan-2-one: LfCS002 Pipecolic acid, L: FrCS030
Nona- trans-2-cis-4-dien-1-al: LfCS002 Pipecolic acid: LfCS037, FrCS037
Nona- trans-2-cis-6-dien-1-al: LfCS002 Polysaccharide T-B: LfCS111
Nona-trans-2-en-1-al: LfCS002 Procyanidin B-2 3'-O-gallate: Lf 166.7CS140
Nona-trans-2-trans-4-dien-1-al: LfCS002 Procyanidin B-2, 3-3'-di-O-gallate: Lf
Oct-1-en-3-ol: LfCS068 0.00084–0.13%CS008,CS010
Octa-1-5-7-trien-3-ol, 3(S)-7-dimethyl: Procyanidin B-2: Lf 5.8CS008
Lf EOCS132 Procyanidin B-3, 3-O-gallate: LfCS070
Octa-1-5-diene-3-7-diol, 3(S)-7-dimethyl, Procyanidin B-3: Lf 0.21%CS010
(+): Lf EOCS132 Procyanidin B-4, 3'-O-gallate: Lf 141CS140
Octan-2-one: LfCS002 Procyanidin B-4: Lf 46.6CS008
Octan-3-ol: LfCS068 Procyanidin B-5, 3-3'-di- O-gallate: Lf 2.6CS008
Octanoate, ethyl: LfCS002 Procyanidin C-1: LfCS010
Octanoate, methyl: LfCS002 Prodelphinidin A-2, 3'-O-gallate: Lf 4.4CS008
Octa-trans-2-cis-4-dien-1-al: LfCS002 Prodelphinidin B-2, 3'-O-gallate: Lf 238CS008
Octa-trans-2-trans-4-dien-1-al: LfCS002 Prodelphinidin B-2, 3-3'-di-O-gallate:
Octa-trans-3-cis-5-dien-2-one: LfCS002 Lf 18.4CS008
Oct-trans-2-enoic acid: LfCS002 Prodelphinidin B-2,3'-O-gallate: Lf 147.4CS140
Oleic acid: Sd oilCS134, LfCS069 Prodelphinidin B-4, 3'-O-gallate:
Oolonghomobisflavan A: Lf 10.6CS008 Lf 63.8–1200CS008,CS010
Oolonghomobisflavan B: Lf 7.2CS008 Prodelphinidin B-4: Lf 56.8–800CS008,CS010
Oolongtheanin: Lf 1.8CS006 Prodelphinidin B-5, 3-3'-di-O-gallate:
Oxalic acid: Lf 1.0%CS144 Lf 29.8CS008
Palmitic acid: Sd oilCS134, LfCS069 Proline, hydroxy: LfCS037, FrCS037
Pedunculagin: LfCS041 Propionamide, N-ethyl: LfCS027
Pent-1-en-3-ol: LfCS068, Sh 0.21–0.23%CS100 Propiophenone, 2-4-dimethyl: LfCS027
Pent-2-en-1-al, 4-methyl-2-phenyl: LfCS002 Propiophenone, para-ethyl: LfCS027
Pentadecane, 2-6-10-14-tetramethyl: LfCS091 Prunasin: LfCS059
Pentan-1-ol: Sh 0.06–0.11%CS100 Pyrazine, 2-3-dimethyl: LfCS027
Pentan-2-ol, methyl: LfCS068 Pyrazine, 2-5-dimethyl: LfCS027
Pentan-3-ol, methyl: LfCS068 Pyrazine, 2-6-dimethyl: LfCS027
Pentanoic acid: 2-amino-5-(N-ethyl- Pyrazine, 2-ethyl-3-5-dimethyl: LfCS027
carboxamido): Lf 120CS105 Pyrazine, 2-ethyl-3-6-dimethyl: LfCS036
Pent-cis-2-en-1-ol: Sh 0.1-0.14%CS100 Pyrazine, 2-ethyl-5-methyl: LfCS027
Pent-cis-3-en-1-al: LfCS002 Pyrazine, 2-ethyl-6-methyl: LfCS027
Phenol: LfCS003 Pyrazine, ethyl: LfCS027
Phenyl, acetate, ethyl: LfCS002 Pyrazine, methyl: LfCS027
Phenyl, acetate, hexyl: LfCS002 Pyrazine, trimethyl: LfCS027
Phenylacetic acid: LfCS002 Pyridine, 2-5-dimethyl: LfCS027
8 MEDICINAL PLANTS OF THE WORLD

Pyridine, 2-6-dimethyl: LfCS027 Tannic acid: Lf CS126

Pyridine, 2-acetyl: LfCS036 Tannin: LfCS024
Pyridine, 2-ethyl: LfCS027 Taraxasterol, Pseudo: Sd oilCS095
Pyridine, 2-ethyl-5-methyl: LfCS036 Taraxerol: Sd oil 20CS095
Pyridine, 2-ethyl-6-methyl: LfCS036 Tartaric acid: LfCS086
Pyridine, 2-methyl: LfCS027 Tea polysaccharides: LfCS055
Pyridine, 2-phenyl: LfCS027 Teasaponin B-1: LfCS057
Pyridine, 3-ethyl: LfCS027 Teasaponin B-2: LfCS040
Pyridine, 3-methoxy: LfCS036 Teasaponin B-3: LfCS040
Pyridine, 3-methyl: LfCS027 Teasaponin B-4: LfCS040
Pyridine, 3-N-butyl: LfCS036 Teasterone: LfCS090
Pyridine, 3-phenyl: LfCS027 Tectoquinone: RtCS039
Pyridine, 4-methyl: LfCS027 Terpineol, 4: LfCS002
Pyridine, 4-vinyl: LfCS036 Terpineol, D: Sh 0.07–0.1%CS100, LfCS068
Pyridine: LfCS027 Theacitrin A: Lf 0.08%CS016
Quercetin: LfCS026, ShCS094 Theaflagallin, epi, 3-O-gallate: Lf 17CS008
Quercetin-3-glucosyl(1-3)rhamnosyl Theaflagallin-3-O-gallate, epi: Lf 0.02%CS010
(1-6)galactoside: LfCS009 Theaflavate B: LfCS019
Quercetin-fructosyl-glucoside: LfCS063 Theaflavic acid, epi, gallate: LfCS064
Quercimeritrin: LfCS026 Theaflavic acid, epi: LfCS064
Quercitrin, iso: LfCS133 Theaflavin, digallate: LfCS071
Quercitrin: LfCS058 Theaflavin, iso: 3'-O-gallate: Lf 25CS019
Quinic acid, (–): LfCS104 Theaflavin, monogallate A: LfCS071
Quinoline, 2-4-dimethyl: LfCS027 Theaflavin, monogallate B: LfCS071
Quinoline, 2-6-dimethyl: LfCS027 Theaflavin, monogallate: LfCS124
Quinoline, 2-methyl: LfCS036 Theaflavin, neo: 3-O-gallate: Lf 30CS019
Quinoline, 3-N-butyl: LfCS027 Theaflavin: LfCS046, Sh 1.12–1.40%CS100,
Quinoline, 3-N-propyl: LfCS027 FlCS159
Quinoline, 4-8-dimethyl: LfCS027 Theaflavin-3'-gallate: LfCS046
Quinoline, 6-methyl: LfCS036 Theaflavin-3'-O-gallate: FlCS159,
Rutin: LfCS058 Lf 18.6–800CS008,CS010
Safranal: LfCS002 Theaflavin-3-3'- digallate: FlCS159
Safrole: LfCS002 Theaflavin-3-3'-di-O-gallate:
Salicylic acid: Headspace volatileCS044 Lf 18.2–300CS008,CS010
Sesquiphelandrene, b: LfCS109 Theaflavin-3-gallate: LfCS046
Sitosterol, E: Sd oilCS134 Theaflavin-3-O-gallate: FlCS159,
Spinasterol, 22-23-dihydro: Sd oilCS131 Lf 6-700CS008,CS010
Spinasterol, D, E-D-glucoside: RtCS039 Theaflavin-monogallate A: LfCS085
Spinasterol, D: RtCS039 Theaflavin-monogallate B: LfCS085
Spinasterol: Sd oilCS131 Theaflavonin, degalloyl: Lf 17.5CS010
Spinasterone, 22-23-dihydro: Sd oilCS131 Theaflavonin: Lf 11.5CS010
Spinasterone: Sd oilCS131 Theanaphthoquinone: LfCS023
Stearic acid: Sd oilCS134 Theanine: LfCS052, Call TissCS066, Seedling Rt
Stigmasterol: Sd oilCS134 109, Sh 63, Cy 577 mg%CS097, St Call
Strictinin: Lf 0.01%CS010 0.37 ppt, An 1.6-2.9%, St 34.9 pptCS099
Succinic acid: LfCS086 Thearubigin: Sh 13.56–15.74%CS100, LfCS139
CAMELLIA SINENSIS 9

Theasapogenol A, 22-O-angeloyl: SdCS020 Undeca-trans-2-en-1-al: LfCS002

Theasapogenol B, 22-O-angeloyl: SdCS020 Urea: PlCS033
Theasapogenol E, 22-O-angeloyl: SdCS020 Vitamin K-1: Lf 3.1-16.5CS072,
Theasaponin B-1: LfCS081 Vitexin, iso, 2''-O-glucoside: LfCS103
Theasaponin E-1: Sd 75CS017 Vitexin: ShCS096
Theasaponin E-2: Sd 10CS017 Vomifeliol, dehydro: Lf EOCS132
Theasaponin, gluco: SdCS061 PHARMACOLOGICAL ACTIVITIES
Theasaponin: SdCS127, LfCS142
AND CLINICAL TRIALS
Theasinensin A: Lf 0.01866–4.8718%CS006,CS140
Antibacterial activity. Alcohol extract of
Theasinensin B: Lf 128.2–600CS140,CS010
black tea, assayed on Salmonella typhi and
Theasinensin C: Lf 70.2CS006
Salmonella paratyphi A, was active on all
Theasinensin D: Lf 17.6CS006
strains of Salmonella paratyphi A, and only
Theasinensin E: Lf 14.4CS006
42.19% of Salmonella typhi strains were
Theasinensin F: Lf 19.6CS006
inhibited by the extract CS048. Hot water
Theasinensin G: Lf 8CS006
extract of the dried entire plant and the tan-
Theaspirane, dihydro, 6-7-epoxy: LfCS002
nin fraction, on agar plate, were active on
Theaspirane, dihydro, 6-hydroxy: LfCS002
Escherichia coli, Pseudomonas aeruginosa, and
Theaspirane: LfCS002
Staphylococcus aureusCS160.
Theaspirone: Lf EOCS132 Anticancer activity. Catechin, adminis-
Theobromine: LfCS029, Call TissCS050, Sd, tered to pheochromocytoma cells in cell
PcCS102, Fl Bd, FlCS107, Petal, Pistil, culture, was active. The cells were incu-
StamenCS117, An, St, St CallCS099, PlCS033, bated with different concentrations of cat-
SeedcoatCS102 echin at short-term (2 days) and long-term
Theogallin: Lf 6-55.5CS008,CS010 (7 days) in Dulbecco’s modified Eagle
Theophylline: SdCS093 medium. The activity of superoxide dismu-
Thiazole, 2-4-5-trimethyl: LfCS036 tase was measured and its mRNA assayed by
Thiazole, 2-4-dimethyl: LfCS036 Northern blotting. After incubation for 2
Thiazole, 2-4-dimethyl-4-ethyl: LfCS036 days, catechin significantly increased the
Thiazole, 2-5-dimethyl: LfCS036 activity of copper/zinc superoxide dismu-
Thiazole, 5-methyl: LfCS036 tase. However, it did not produce significant
Thymol: LfCS002 effect at 7 days. The magnesium superoxide
Tirucalla-7-24-dien-3-E-ol, 5-D: dismutase activity produced significant
Sd oil 12CS062 changes in both short- and long-term treat-
Tirucalla-7-24-dien-3-E-ol: Sd oilCS095 ment groups. The amount of mRNA also
Tirucallol: Sd oilCS095 showed similar changesCS040.
Toluidine, ortho: LfCS027 Anticarcinogenic activity. The anticar-
Triacontan-1-ol: LfCS075 cinogenic activity of tea phenols has been
Tricetin: ShCS094 demonstrated in rats and mice transplant-
Tricetinidin: LfCS139 able tumors, carcinogen-induced tumors in
Trifolin: LfCS058 digestive organs, mammary glands, hepato-
Tr-saponin A: Rt 2.2CS022 carcinomas, lung cancers, skin tumors, leu-
Tr-saponin B: Rt 5.9CS022 kemia, tumor promotion, and metastasis.
Tr-saponin C: Rt 2.8CS022 The mechanisms of this effect indicated
Typhasterol: LfCS090 that the inhibition of tumors may be the
Umbelliferone: LfCS032 result of both extracellular and intracellular
Undeca-2-one, 6-10-dimethyl: LfCS002 mechanisms indicating the modulation of
10 MEDICINAL PLANTS OF THE WORLD

metabolism, blocking or suppression, modu- blotting methodsCS020. Green and black tea,
lation of DNA replication and repair effects, administered orally to hairless mice in the
promotion, inhibition of invasion and absence of any chemical initiators or pro-
metastasis, and induction of novel mechan- moters, resulted in significantly fewer skin
ismsCS002. The association of green tea and papillomas and tumors induced by UVA
cancer has been investigated in 8552 Japa- and UVB light. Black tea however, provided
nese women 40 years of age. After 9 years of better protection against UVB-induced
follow-up study, 384 cases of cancer were tumors than green tea. Black tea consump-
identified. There was a negative association tion was associated with a reduction in the
between cancer incidence and green tea number of sunburn cells in the epidermis of
consumption, especially among females mice 24 hours after irradiation, although
consuming more than 10 cups of tea a day. there was no effect of green tea. Other indi-
A slow down in increases of cancer inci- ces of early damage such as necrotic cells or
dence with age was observed among females mitotic figures were not affected. Neutro-
who consumed more than 10 cups phil infiltration as a measure of skin redness
daily CS010 . Tea, taken by lung cancer was slightly lowered by tea consumption in
patients at a dose of two or more cups per the UVB groupCS023. Epigallocatechin-3-
day, reduced the risk by 95%. The protected gallate, in cell culture, activated proMMP-
effect was more evident among Kreyberg I 2 in U-87 glioblastoma cells in the presence
tumors (squamous cell and small cells) and of concanavalin A or cytochalasin D, two
among light smokersCS011. The green tea potent activators of MT1-MMP, resulted in
polyphenols, epi-gallocatechin-3-gallate, proMMP-2 activation that was correlated
applied topically to human skin, prevented with the cell surface proteolytic processing
penetration of ultraviolet (UV) radiation. of Mt1-MMP to it’s inactive 43 kDa form.
This was demonstrated by the absence of Addition of epigallocatechin-3-gallate
immunostaining for cyclobutane pyrimidine strongly inhibited the MT1-MMP-driven
dimers in the reticular dermis. Topical migration in the cells. The treatment of
administration to the skin of mice inhi- cells with non-cytotoxic doses of epigal-
bited UVB-induced infiltration of CDIIb+ locatechin-3-gallate significantly reduced
cells. The treatment also results in re- the amount of secreted pro MMP-2, and led
duction of the UVB-induced immuno- to a concomitant increase in intracellular
regulatory cytokine interleukin (IL)-10 in levels of that protein. The effect was similar
the skin and draining lymph nodes, and an to that observed using well-characterized
elevated amount of IL-12 in draining lymph secretion inhibitors such as brefeldin A and
nodesCS015. Green tea extract, in human manumycin, indicative that epigallo-
umbilical vein endothelial cells, did not catechin could also potentially act on intra-
affect cell viability but significantly reduced cellular secretory pathwaysCS044. Green tea
cell proliferation dose-dependently and pro- polyphenols, at a dose of 30 mg/mL, inhi-
duced a dose-dependent accumulation of bited the photolabeling of P-glycoprotein
cells in the gastrointestinal phase. The de- (P-gp) by 75% and increased the accumula-
crease of the expression of vascular tion of rhodamine-123 in the multidrug-re-
endothelial growth factor receptors fms-like sistant cell line CH(R)C5. This result
tyrosine kinase and fetal liver kinase-I/ indicated that green tea polyphenols inter-
kinase insert domain containing receptor in act with P-gp and inhibited its transport
the cell culture by the extract was detected activity. The modulation of P-gp was a
with immunohistochemical and Western reversible process. Epigallocatechin-3-gal-
CAMELLIA SINENSIS 11

late potentiates the cytotoxicity of vinblas- nidermatum, and Rhizopus stolonifer CS162.
tine in CH(R)C5 cells. The inhibitory ef- Saponin fraction of the leaf on agar plate
fect on P-gp was also observed in human was active on Microsporum audonini,
Caco-2 cellsCS045. minimum inhibitory concentration (MIC)
Anticataract activity. Tea, administered in 10 mg/mL; Epidermophyton floccosum and
culture to enucleated rat lens, reduced the Trichophyton mentagrophytes, MICs 25 Pg/
incidence of selenite cataract in vivo. The mLCS165.
rat lenses were randomly divided into nor- Antihypercholesterolemic activity. Tea
mal, control and treated groups and incu- supplemented with vitamin E, administered
bated for 24 hours at 37qC. Oxidative stress to male Syrian hamsters, reduced plasma
was induced by sodium selenite in the cul- low-density lipoprotein (LDL) cholesterol
ture medium of the two groups (except the concentrations, LDL oxidation, and early
normal group). The medium of the treated atherosclerosis compared to the consump-
group was additionally supplemented with tion of tea alone by the hamsters. The anti-
tea extract. After incubation, lenses were oxidant action of vitamin E is through the
subjected to glutathione and malondial- incorporation of vitamin E into the LDL
dehyde estimation. Enzyme activity of molecule. The hamsters were fed a semi-
superoxide dismutase, catalase, and glu- purified hypercholesterolemic diet contain-
tathione peroxidase were also measured in ing 12% coconut oil, 3% sunflower oil, and
different sets of the experiment. In vivo 0.2% cholesterol (control), control and
cataract was induced in 9-day-old rat pups 0.625% tea, control and 1.25% tea or con-
of both control and treated groups by a trol and 0.044% tocopherol acetate for 10
single subcutaneous injection of sodium weeks. The hamsters fed the vitamin E diet
selenite. The treated pups were injected compared to the different concentrations
with tea extract intraperitoneally prior to of tea significantly lower plasma LDL cho-
selenite challenge and continued for 2 con- lesterol concentrations, –18% (p < 0.007),
secutive days thereafter. Cataract incidence –17% (p < 0.02), and –24% (p < 0.0001),
was evaluated on 16 postnatal days by slit respectively. Aortic fatty streak areas were
lamp examination. There was positive reduced in the vitamin E diet group com-
modulation of biochemical parameters in pared to the control, –36% (p < 0.04) and
the organ culture study. The results indi- low tea –45% (p < 0.01) diets. Lag phase of
cated that tea act primarily by preserving conjugated diene production was greater in
the antioxidant defense systemCS039. the vitamin E diet compared to the control,
Antidiarrheal activity. Hot water extract low tea, and high tea diets, 41% (p <
of tea, administered orally to rats, was effec- 0.0004), 40% (p < 0.0004), and 39% (p <
tive in all the models of diarrhea used. 0.0008), respectively. Rate of conjugated
Naloxone (0.5 mg/kg, ip) and loperamide diene production was reduced in the
significantly inhibited the antidiarrheal vitamin E diet compared to the control, low
activity of the extractCS029. tea, and high tea diets, –63% (p < 0.002),
Antifungal activity. Ethanol (50%) extract –57% (p < 0.005), and –59% (p < 0.02),
of the entire plant, in broth culture at a con- respectively CS005. Infusion of black tea
centration of 1 mg/mL, was inactive on leaves was taken by 31 men (ages 47 r 14)
Aspergillus fumigatus and Trichophyton men- and 34 females (ages 35 r 13) in a 4-week
tagrophytesCS161. Hot water extract of the leaf study. Six mugs of tea were taken daily vs
on agar plate at a concentration of 1.0% was placebo (water, caffeine, milk, and sugar)
active on Alternaria tenuis, Pythium apha- and blood lipids, bowel habit, and blood
12 MEDICINAL PLANTS OF THE WORLD

pressure measured during a run-in period p38-MAPK in chondrocytes. Epigallo-

and at the end weeks 2, 3, and 4 of the test catechin-3-gallate did not alter the total
period. Compliance was established by add- nonphosphorylated levels of either p38-
ing a known amount of p-aminobenzoic acid MAPK or ERKp44/p42 in osteoarthritis
to selected tea bags and then measure it chondrocytesCS033. Epigallocatechin-3-gal-
excretion in the urine. Mean serum choles- late administered to primary human
terol values during run-in, placebo and on osteoarthritis chondrocytes at a concentra-
tea drinking were 5.67 r 1.05, 5.76 r 1.11, tion of 100 PM in cell Culture, inhibited the
and 5.69 r 1.09 mmol/L (p = 0.16). There IL-I E-induced production of nitric oxide by
were also no significant changes in diet, interfering with the activation of nuclear
LDL-cholesterol, high-density lipoprotein factor (NF)NBCS042. Tea, in culture with
(HDL) cholesterol, triacylglycerols, and bovine nasal and metacarpophalangeal
blood pressure in the tea intervention cartilage and human nondiseased osteoar-
period compared with placebo. Stool con- thritis and rheumatoid cartilage with and
sistency was softened with tea compared without reagents known to accelerate carti-
with the placebo, and no other differ- lage matrix breakdown, produced chon-
ences were observed in bowel habit. The droprotective effect that may be beneficial
results were unchanged within 15 “non- for the arthritis patient by reducing inflam-
compliers” whose p-aminobenzoic acid mation and the slowing of cartilage break-
excretion indicated that fewer than six tea down. Individual catechins were added to
bags had been used, were excluded from the the cultures and the amount of released
analysis, and when differenced between proteoglycan and type II collagen were mea-
run-in and tea periods were considered sepa- sured by metachromatic assay and inhibi-
rately for those who were given tea first or tion enzyme-linked immunosorbent assay
secondCS167. (ELISA), respectively. Possible nonspecific
Anti-inflammatory effect. Epigallocate- or toxic effects of the catechins were
chin-3-gallate was shown to mimic its anti- assessed by lactate output and proteoglycan
inflammatory effects in modulating the synthesis. Catechins, particularly those
IL-I E-induced activation of mitogen acti- containing a gallate ester, were effective
vated protein kinase in human chondro- at micromolar concentrations at inhibiting
cytes. It inhibited the IL-I E-induced proteoglycan and type II collagen break-
phosphorylation of c-Jun N-terminal kinase downCS043.
(JNK) isoforms, accumulation of phospho- Antimutagenic activity. The anticarcino-
c-Jun and DNA-binding activity of AP-1 in genic activity of tea phenols has been
osteoarthritis chondrocytes, IL-I E but not demonstrated in rats and mice, transplant-
epigallocatechin-3-gallate, and induced the able tumors, carcinogen-induced tumors in
expression of JNK p46 without modulating digestive organs, mammary glands, hepato-
the expression of JNK p54 in osteoarthritis carcinomas, lung cancers, skin tumors, leu-
chondrocytes. In immune complex kinase kemia, tumor promotion, and metastasis.
assays, epigallocatechin-3-gallate com- The mechanisms of this effect indicated
pletely blocked the substrate phosphorylat- that the inhibition of tumors maybe the
ing activity of JNK but not p38-mitogen result of both extracellular and intracellular
activated protein kinase (MAPK). Epigallo- mechanisms indicting the modulation of
catechin-3-gallate had no inhibitory effect metabolism, blocking or suppression, modu-
on the activation of extracellular signal- lation of DNA replication and repair effects,
regulated kinase p44/p42 (ERKp44/p42) or promotion, inhibition of invasion and
CAMELLIA SINENSIS 13

Metastasis, and induction of novel mech- tagenic potency compared with the corre-
anismsCS002. Green and black teas, adminis- sponding artificial teaCS019. Green and black
tered orally to human adults, were effective. tea polyphenols, applied to the surfaces of
Between 60 and 180 minutes after the teas ground beef before cooking, inhibited the
were administered, the antimutagenic formation of the mutagens in a dose-related
active compounds were recovered from the fashionCS025. Green or black tea polyphe-
jejunal compartment by means of dialysis. nols sharply decreased the mutagenicity of a
The dialysate appeared to inhibit the mu- number of aryl- and heterocyclic amines, of
tagenicity of the food mutagen 2-amino-3,8- aflatoxin B1, benzo[a]pyrene, 1,2-dibromo-
dimethylimidazo[4,5-f]quinoxaline on ethane, and more selectively of 2-nitropro-
Salmonella typhimurium. The maximum pane, all involving an induced rat liver S9
inhibition was measured at 2 hours after fraction. Good inhibition was found with
administration and was comparable for two nitrosamines that required a hamster S9
black and green teas. The maximum inhibi- fraction for biochemical activation. No
tion observed with black tea was reduced by effect was found with 1-nitropyrene and
22, 42, and 78% in the presence of whole with the direct-acting (no S9) 2-chloro-4-
milk, semi-skimmed milk, and skimmed methyl-thiobutanoic acidCS027. Hot water
milk, respectively. Whole milk and skimmed extract on the leaf was evaluated in cell cul-
milk abolished the antimutagenic activity of tures on various systems vs decaffeinated
green tea by more than 90% and semi- and caffeinated teas. On mouse mammary
skimmed milk by more than 60%. When a gland vs decaffeinated and caffeinated teas,
homogenized breakfast was taken with black ICs50 were 10 mg/mL and 10 Pg/mL on CA-
tea, the antimutagenic activity was elimi- A427, IC50 27 mg/mL and 31 Pg/mL, and
nated. When tea and mutagen 2-amino-3,8- on epithelial cells, IC50 0.01 ng/mL and 0.3
dimethylimidazo[4,5-f]quinoxaline were ng/mLCS169. Hot water extract of the leaf,
added to the system, 2-amino-3,8-dimethyl- on agar plate at a concentration of 1 mg/
imidazo[4,5-f]quinoxaline mutagenicity was plate, was active on Salmonella typhimu-
efficiently inhibited, with green tea show- rium TA98 vs 2-amino-3-methylimidazo
ing a slightly stronger antimutagenic activ- [4,5-f]quinoline-induced mutagenesis and
ity than black tea. The addition of milk had produced weak activity vs benzo[a]pyrene-
only a small inhibiting effect on the induced mutagenesisCS168. Infusion of the
antimutagenicity. The antimutagenic activ- leaf, on agar plate at a concentration of 0.7
ity corresponded with reduction in antioxi- mg/plate, was active on Salmonella typhimu-
dant capacity and with a decrease of rium TA98 and TA100 vs 2-amino-3-
concentration of catechin, epigallocatechin methylimidazo[4,5-f]quinoline-;
gallate, and epigallocatechinCS014. Chinese 3-amino-1,4-dimethyl-5H-pyrid[4,3-
white tea, tested on rat liver S9 in assay for b]indole(Trp-1); aflatoxin B1-; 2-amino-6-
methoxyresorufin O-demethylase, inhibited methyl-dipyrido[1,2-A:3,2-d]imidazole-,
methoxyresorufin O-demethylase activity and benzo[a]pyrene-induced carcinogen-
and attenuated the mutagenic activity of esisCS170. Infusion of the leaf, on agar plate
3-methylimidazo[4,5-f]quinoline (IQ) in at a concentration of 50 mg/plate, was
absence of S9. Nine of the major constitu- active on Salmonella typhimurium TA98 vs
ents found in green and white teas were 2-amino-3-methylimidazo[4,5-f]quinoline-;
mixed to produce artificial teas according to 2-amino-3,4-dimethyl-imidazo[4,5-
their relative levels in white and green teas. f]quinoline-;2-amino-3,8-dimethylimi-
The complete tea exhibited higher antimu- dazo[4,5-f]quinoxaline-;
14 MEDICINAL PLANTS OF THE WORLD

2-amino-1-methyl-6-phenylimidazo[4,5-b]- in urine and lowered the esterified and total

pyridine-;2-amino-3,7,8- cholesterol contents in plasma as compared
trimethylimidazo[4,5-f]quinoxaline-; with a control group. TBARS contents in
2-amino-3,4,7,8-tetramethyl-3H-imidazo- liver, plasma, and cholesterol levels in the
[4,5-f]quinoxaline-inoxaline-; 3-amino-1,4- liver were not affected. The lower plasma
dimethyl-5H-pyrid[4,3-b]indole cholesterol concentration could not be
(Trp-P-I)- and 3-amino-1-methyl-5H- explained by increased fecal excretion of
pyrido [4,3-b]indole-induced mutagenesis. cholesterol or bile acids. On the other hand,
Metabolic activation was required for posi- a relationship between decreased plasma
tive resultsCS171. cholesterol and significantly higher acetate
Anti-neoplastic effect. Green tea, admin- concentrations in the cecum, colon, and
istered orally at a dose of 6 g per day in six portal blood of rats was assumed. Copper
doses to 42 patients who were asymptom- absorption was significantly increased while
atic and had manifested, progressive iron absorption was not affected CS007 .
prostate specific antigen elevation with Epigallocatechin gallate, tea polyphenols,
hormone therapy, produced limited anti- and tea extract were added to human plasma
neoplastic activity. Continued use of lutein- and lipid peroxidation induced by the
izing hormone-releasing hormone agonist water-soluble radical generator 2,2'-azobis
was permitted. However, patients were (2-amidinopropane) dihydrochloride. Fol-
ineligible if they had received other treat- lowing a lag phase, lipid peroxidation was
ments for their disease in the preceding 4 initiated and it occurred at a rate that was
weeks or if they had received a long-acting lower in a dose that was lowered in a dose-
antiandrogen therapy in the preceding 6 dependent manner by the polyphenols.
weeks. The patients were monitored Similarly, epigallocatechin gallate and the
monthly for response and toxicity. Tumor extract added to plasma strongly inhibited
response, defined as a decline of 50% or 2,2'-azobis(2-amidinopropane)
greater in the baseline prostate-specific dihydrochloride-induced lipid peroxidation.
antigen (PSA) value, occurred in a single The lag phase preceding detectable lipid
patient, or 2% of The cohort (95% confi- peroxidation was the result of the antioxi-
dence interval [CI], 1–14%). This one dant activity of endogenous ascorbate,
response was not sustained beyond 2 which was more effective at inhibiting lipid
months. At the end of the first month, the peroxidation than the tea polyphenols and
median change in the PSA value from was not spared by these compounds. When
baseline for the cohort increased by eight volunteers consumed the equiva-
43%CS031. Infusion of the leaf, administered lent of six cups of tea, the resistance of
in the drinking of female mice at a concen- their plasma to lipid peroxidation did not
tration of 1.25%, was active vs UV radia- increase over a period of 3 hoursCS009. Black
tion-induced papillomas and tumorsCS172. tea leaves, administered to human red blood
Leaves in the drinking water of female mice cells, was effective against damage by oxi-
at a dose of 0.6% reduced lung tumor multi- dative stress induced by inducers such as
plicity and volume in 4-(methylnitro- phenylhydrazine, Cu2+-ascorbic acid, and
samine)-1-(3-pyridyl)-1-butanone (NNK) xanthine/xanthine oxidase systems. Lipid
treated miceCS173. peroxidation of pure erythrocyte membrane
Antioxidative effect. Tea, administered and of whole red blood cell was completely
orally to rats, decreased the thiobarbituric prevented by black tea extract. Similarly,
acid reactive substances (TBARS) contents the tea provided total protection against
CAMELLIA SINENSIS 15

degradation of membrane proteins. Mem- Antispasmodic activity. Hot water extract

brane fluidity studies as monitored by the and tannin fraction of the dried entire plant
fluorescent probe 1,6-diphenyl-hexa-1,3,5- were active on the rabbit and rat intestines
triene showed considerable disorganization vs pilocarpine-induced spasms and barium-
of its architecture that could be restored induced contractionsCS160.
back to normal on addition of black tea or Antiviral activity. Epigallocatechin-3-gal-
free catechins. The tea extract in compari- late, administered to Hep2 cells in culture,
son to free catechin seemed to be a better produced a therapeutic index of 22 and an
protecting agent against various types of IC 50 of 25 PM. The agent was the most
oxidative stressCS013. Ethanol/water (7:3) effective when added to the cells during the
extract of green tea, tested on 2,2-azino-di- transition from the early to the late phase of
3-ethylbenzthiazoline sulphonate, produced viral infection suggesting that the polyphe-
antioxidant activity compared with that nol inhibits one or more late steps in virus
of ascorbic acid (10 mmol/L)CS018 . The infectionCS016.
Nonpolyphenolic fraction of residual green Ethanol (50%) extract of the entire plant,
tea (after hot water extraction) produced a in broth culture at a concentration of 50 Pg/
significant suppression against hydroperox- mL, was inactive on Raniket and Vaccinia
ide generation from oxidized linoleic acid in virusesCS161. Hot water extract of the leaf in
a dose-dependent manner. Using silica gel
cell culture was active on Coxsackie A9, B1,
TLC plate, chlorophylls a and b, pheo-
B2, B3, B4, and B6 viruses, Echo type 9
phytins a and b, E-carotene, and lutein were
virus, herpes simplex virus, poliovirus III,
isolated. All of these constituents exhibited
vaccinia virus, and REO type 1 virusCS163.
significant antioxidant activites, the ranks
Anti-yeast activity. Ethanol (50%) extract
of suppressive activity against hydroperox-
of the entire plant, in broth culture at a
ide generation were chlorophyll a > lutein
> pheophytin a > chlorophyll b > b-caro- concentration of 1 mg/mL, was inactive on
tene > pheophytin bCS047. Candida albicans, Cryptococcus neoformans,
Antiproliferative activity. Green tea frac- and Sporotrichum schenckii CS161. Ethanol
tions, tested on human stomach cancer extract of the leaf on agar plate produced
(MK-1) cells, indicated six active flavan-3- MIC 9.3 mg/mL on Candida albicans CS164.
ols, epicatechin, epigallocatechin, epigal- Coronary heart disease prevention. Tea,
locatechin gallate, gallocatechin, epicatechin taken by men and women age 30 to 70 years
gallate, and gallocatechin gallate. Among at a dose of 480.0 mL per day, produced a
the six active flavan-3-ols, epigallocatechin positive dose–response effectCS008.
gallate and gallocatechin gallate produced Cytochrome P50 expression. Fresh leaves
the highest activity. Epigallocatechin, of green, black, and decaffeinated black tea
gallocatechin, and epicatechin gallate fol- enhanced lauric acid hydroxylation. The
lowed next, and the activity of epicatechin decaffeinated black tea produced no signifi-
was lowest. This suggests that the presence cant effect. Green tea and black tea but not
of the three adjacent hydroxyl groups decaffeinated black tea, stimulated the O-
(pyrogallol or galloyl group) in the molecule dealkylations of methoxy-, ethoxy-, and
would be a key factor for enhancing the pentoxy-resorufin indicating upregulation
activityCS032. of cytochrome P50 (CYP)1A and CYP2B.
Antiprotozoan activity. Ethanol (50%) Immunoblot analysis revealed that green
extract of the entire plant, in broth culture and black tea, but not decaffeinated black
at a concentration of 125 Pg/mL, was inac- tea, elevated the hepatic CYP1A2 apopro-
tive on Entamoeba histolyticaCS161. tein levels. Hepatic microsomes from green
16 MEDICINAL PLANTS OF THE WORLD

and black tea-treated rats, but not those for tea and salivary pellicle components.
from the decaffeinated black tea-treated Thirty-four percent of the fluoride was
rats, were more effective than controls in retained in the oral cavity. Differences in
converting IQ into mutagenic species in the retention at the tooth surface in the pres-
Ames testCS001. ence and absence of an acquired pellicle
Dental enamel erosion. Herbal tea and were not statistically significant at incisor
conventional black tea, tested on teeth, or molar sites. Fluoride from tea showed
resulted in erosion of dental enamel. After strong binding to enamel particles, which
exposure to tea, sequential profilometric was only partially dissociated by solutions of
tracings of the specimens were taken, super- ionic strength considerably greater than
imposed, and the degree of enamel loss cal- that of salivaCS012.
culated as the area of disparity between the Gastrointestinal effect. Green tea, admin-
tracings before and after exposure. Tooth istered to rats fasted for 3 days, reverted to
surface loss resulted from herbal tea (mean normal the mucosal and villous atrophy
0.05 mm2) was significantly greater than induced by fasting. Black tea ingestion had
that which resulted from exposure to con- no effect. Ingestion of black tea, green tea,
ventional black tea (0.01 mm2), and water and vitamin E before fasting protected the
(0.00 mm2)CS022. Tannin, catechin, caffeine, intestinal mucosa against atrophyCS003. Char-
and tocopherol, tested in vitro on tooth acterization of melanin extracted from tea
enamel, demonstrated that these compo- leaves proved similarity of the original com-
nents possess the property of increasing the pound to standard melanin. The Langmuir
acid resistance of tooth enamel. The effects adsorption isotherms for gadolinium (Gd)
increased dramatically when the compo- binding were obtained using melanin. Mela-
nents were used in combination with fluo- nin–Gd preparation demonstrated low
ride. A mixture of tannic acid and fluoride acute toxicity. LD50 for the preparation was
showed the highest inhibitory effect (98%) in a range of 1.25–1.50 g/kg in mice. Mag-
on calcium release to an acid solution. Tan- netic resonance imaging (MRI) properties
nin in combination with fluoride inhibited of melanin itself and melanin-Gd com-
the formation of artificial enamel lesions in plexes have been estimated. Gadolinium-
comparison with acidulated phosphate free melanin fractions possess slighter
fluoride (APF) as determined by electron relaxivity compared with its complexes. The
probe microanalysis, polarized-light micros- relaxivity of lower molecular weight frac-
copy, and Vickers microhardness measure- tion was 2 times higher than relaxivity of
mentCS024. Gd(DTPA) standard. Postcontrast images
DNA effect. Green tea extract, in cell cul- demonstrated that oral administration of
ture at a dose of 10 mg/L corresponding to melanin complexes in concentration of
15 mmol/L EGCg for 24 hours, did not pro- 0.1 mM provides essential enhancement to
tect Jurkat cells against H2O2-induced DNA longitudinal relaxation times (T[1])-weigh-
damage. The DNA damage, evaluated by ted spin echo image. The required contrast
the Comet assay, was dose-dependent. and delineation of the stomach wall dem-
However, it reached plateau at 75 mmol/L onstrated uniform enhancement of MRI
of H 2O 2 without any protective effect with proposed melanin complexCS049.
exerted by the extract. The DNA repair Hypocholesterolemic effect. Green tea,
process, completed within 2 hours, was in human HepG2 cell culture, increased
unaffected by supplementationCS021. both LDL receptor-binding activity and
Fluoride retention. Tea, used as a mouth protein. The ethyl acetate extract, contain-
rinse, demonstrated strong avidity of enamel ing 70% (w/w) catechins, also increased
CAMELLIA SINENSIS 17

LDL receptor-binding activity, protein, and the insulin-potentiating activity for green
mRNA, indicating that the effect was at the and oolong teas was owing to epigalloca-
receptor level of gene transcription and that techin gallate. For black tea, the activity
the catechins were the active constituents. was present in addition to epigallocatechin
The mechanism by which green tea gallate, tannins, theaflavins, and other
upregulated the LDL receptor was investi- undefined compounds. Several known com-
gated. Green tea decreased the cell choles- pounds found in tea were shown to enhance
terol concentration (–30%) and increased insulin with the greatest activity due to
the conversion of the sterol-regulated ele- epigallocatechin gallate followed by
ment binding protein (SREBP-1) from the epicatechin gallate, tannins, and thea-
inactive precursor form to the active tran- flavins. Caffeine, catechin, and epicatechin
scription-factor form. Consistent with this, displayed insignificant insulin-enhancing
the mRNA of 3-hydroxy-3-methylglutaryl activities. Addition of lemon to the tea did
coenzyme-A reductase, the rate limiting not affect the insulin-potentiating activity.
enzyme in cholesterol synthesis, was also Addition of 5 g of 2% milk per cup
increased by green teaCS050. decreased the insulin-potentiating activity
Immunomodulatory effect. To determine one-third, and addition of 50 g of milk per
the effects of tea on transplant-related cup decreased the insulin-potentiating
immune function in vitro lymphocyte pro- activity approx 90%. Non-dairy creamers
liferation tests using phytohemagglutinin, and soymilk also decreased the insulin-
mixed lymphocytes culture assay, IL-2, and potentiating activityCS034.
IL-10 production from mixed lymphocyte Iron absorption. Tea, administered by
proliferation were performed. Tea had gastric intubation to rats, did not affect iron
immunosuppressive effects and decreased absorption when tea was consumed for 3
alloresponsiveness in the culture. The days but when delivered in tea the absorp-
immunosuppressive effect of tea was medi- tion was decreased. Rats maintained on a
ated through a decrease in IL-2 produc- commercial diet were fasted overnight with
tion CS038. Tea, assayed in cell culture, free access to water and then gavaged with
enhanced neopterin production in unstimu- 1 mL of 59Fe labeled FeCl3 (0.1 mM or 1 mM)
lated peripheral mononuclear cells, whereas and lactulose (0.5 M) in water or black tea.
an effective reduction of neopterin forma- Iron absorption was estimated from Fe
tion in cells stimulated with concanava- retention. Intestinal permeability was
lin A, phytohemagglutinin or interferon evaluated by lactulose excretion in the
(IFN)-J was observed CS041. Theaflavins urine. Iron absorption was lower with given
potently suppressed IL-2 secretion, IL-2 with tea at both iron concentrations but tea
gene expression, and the activation of did not affect lactulose excretionCS004.
NF-NB in murine spleens enriched for Lipid peroxidation activity. Solubilized
CD4(+) T-cells. Theaflavins also inhibited green tea, administered orally to rats for 5
the induction of IFN-J mRNA. However, weeks, reduced lipid peroxidation products.
the expression of the T(H2) cytokines IL-4 The treatment produced increased activity
and IL-5, which lack functional NF-NB sites of glutathione (GSH) peroxidase and GSH
within their promoters was unexpectedly reductase, increased content of reduced
suppressed by theaflavins as wellCS046. GSH, a marked decrease in lipid hydroper-
Insulin-enhancing effect. Tea, as normally oxides and malondialdehyde in the liver, an
consumed, was shown to increase insulin increase in the concentration of vitamin A
activity more than 15-fold in vitro in an by about 40%. A minor change in the mea-
epididymal fat cell assay. The majority of sured parameters was observed in the blood
18 MEDICINAL PLANTS OF THE WORLD

serum. GSH content increased slightly, group (58.3%) were significantly better
whereas the index of the total antioxidant than that of the control group (13.6%) (p <
status increased significantly. In contrast, 0.005)CS035.
the lipid peroxidation products, particularly P-glycoprotein activity. Green tea poly-
malondialdehyde, was significantly dimin- phenols (30 Pg/mL) inhibited the photo-
ished. In the central nervous tissue, the labeling of P-gp by 75% and increased the
activity of superoxide dismutase and glu- accumulation of rhodamine-123 threefold
tathione peroxidase decreased, whereas the in a multidrug-resistant cell line CH(R)C5,
activity of GSH reductase and catalase indicating that the polyphenols interact
increased after drinking green tea. More- with P-gp and inhibit its transport activity.
over, the level of lipid hydroperoxides, 4- The modulation of P-gp transport by
hydroksynonenal, and malondialdehyde polyphenols was a reversible processCS045.
decreased significantlyCS036. Photoprotection effect. Tea extracts,
Neuromuscular-blocking action. Thearu- administered topically, produced a dose-
bigin fraction of black tea was investigated dependent inhibition of the erythema
for neuromuscular-blocking action of botu- response evoked by UV radiation. The (–)-
linum neurotoxin types A, B, and E in the epigallocatechin-3-gallate and (–)-epica-
mouse phrenic nerve-diaphragm prepara- techin-3-gallate polyphenolic fractions
were most efficient at inhibiting erythema,
tions. On binding, A (1.5 nM), B (6 nM),
whereas (–)-epigallocatechin and (–)-
and E (5 nM) abolished indirect twitches
epicatechin had little effect. On histologi-
within 50, 90, and 90 minutes, respectively.
cal examination, skin treated with the
Thearubigin fraction mixed with each toxin
extracts reduced the number of sunburn
protected against the neuromuscular-block-
cells and protected epidermal Langerhans
ing action of botulinum neurotoxin types A,
cells from UV damage. The extract also
B, and E by binding with the toxinsCS037. reduced damage that formed after UV
Oral submucousal fibrosis effect. Tea, radiation CS006. Green tea polyphenols,
administered orally to 39 patients with oral applied topically to the human skin, pre-
submucous fibrosis, indicated that the treat- vented UVB-induced cyclobutane pyrimi-
ment was effective for patients with abnor- dine dimers, which are considered to be
mal hemorheology. The patients were mediators of UVB-induced immune sup-
divided into control and experimental pression and skin cancer induction. The
groups. The control group included 22 oral treatment, prior to exposure to UVB, pro-
submucous fibrosis patients who were tected against UVB-induced local as well as
treated by oral administration of vitamins A systemic immune suppression in laboratory
and D, vitamin B complex, and vitamin E. animals. Additionally, treatment of mouse
The experimental group included 17 skin inhibited UVB-induced infiltration
patients who were treated with vitamins of CD11b cells. CD11b is a cell-surface
and tea pigment after their examination of marker for activated macrophages and neu-
hemorheology. The results showed that 7 of trophils, which are associated with induc-
12 patients in the experimental group with tion of UVB-induced suppression of contact
abnormal hemorheology had average 7.9 hypersensitivity responses. The treatment
mm improvement on the open degree also resulted in reduction of the UVB-
(58.3%), and the open degree of the other induced immunoregulatory cytokine IL-10
five patients whose hemorheology was in skin as well as in draining lymph nodes,
normal only increased 2 mm (20%). The and an elevated amount of IL-12 in drain-
therapeutical results of the experimental ing lymph nodesCS026.
CAMELLIA SINENSIS 19

Protease inhibition. Epigallocatechin-3- grade 3 toxicity and one episode of grade 4

gallate, in cell culture at a concentration of toxicity also occurred, with the latter mani-
100 PM, reduced virus yield by 2 orders of festing as severe confusionCS031.
magnitude producing an IC50 of 25 PM and Toxicity assessment. Ethanol (50%)
a therapeutic index of 22 in Hep2 cells. The extract of the entire plant, administered
agent was the most effective when added to intraperitoneally to mice produced lethal
the cells during the transition from the early dose (LD)50 316 mg/kgCS161. Ethanol (95%)
to the late phase of viral infection, suggest- extract of the leaf, administered by gastric
ing that it inhibited one or more late steps intubation to mice, produced LD50 10 g/kg.
in virus infection. One of these steps appears Intraperitoneal administration produced
to be virus assembly, because the titer of CD90 0.7 g/kgCS166.
infectious virus and the production of physi-
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cocoa. J Agr Food Chem 1993; component of green tea on the prolif-
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CS075 Narayan, M. S., B. Bhattacharya, N. Camellia sinensis (l.) O. Kuntze for use
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24 MEDICINAL PLANTS OF THE WORLD

CS089 Ikekawa, N., S. Takatsuto, T. Kitsuwa, Effect of plucking intervals on the

H. Saito, T. Morishita and H. Abe. chemical constituents of CTC black
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Analysis of the aroma of Sichuan CS103 Chaboud, A., J. Rayaud, L. Debourcieu
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CS092 Nonaka, G. I., R. Sakai and I. Nishioka. glucosylapigenin or 2”-)-glucosylisovi-
Hydrolysable tannins and proantho- texin in the leaves of Thea sinensis
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CS093 Skhiladze, N. R. and V. Y. Vachnadze. CS104 Sakata, K., S. Sakuraba, A. Yagi, K.
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1984; 20(5): 641. as an unidentified major tea–compo-
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Biol Chem 1984; 48(11): 2861–2862. Camellia sinensis L. Yao Hsueh Hsueh
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CS100 Barruah, S., M. Hhazarika, P. K. oids: brassinone, (24S)-24-etylbrassi-
Mahanta, H. Horita and T. Mutai. none ad 28–norbrassinolide, in higher
CAMELLIA SINENSIS 25

plants. Experientia 1983; 39(4): Chen. Determination of trace germa-

351–353. nium in herbal medicine by graphite fur-
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26 MEDICINAL PLANTS OF THE WORLD

CS131 Itoh, T., Y. Kikuchi, T. Tamura and T. mary and secondary amines in the
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