Issue: 37 Page: 33
Rediscovering Tea: An Exploration of the Scientific Literature.
by Robert L. Gutman, Beung-Ho Ryu
HerbalGram. 1996; 37:33 American Botanical Council
Interest in tea is growing. Scientists now report that tea is good food because it may help prevent some chronic diseases. This article reviews the history of tea as a beverage; the botany and cultivation of the plant; and the chemistry, pharmacology, and health benefits of its active ingredients. Tea polyphenols are described in detail to reflect their potential role in maintaining good health.
A BRIEF HISTORY OF TEA
Chinese legend has it that tea was the accidental discovery of King Shen Nong in about 2700 B.C. (Shouyi, 1982). A clever man, he is also credited with the invention of plowing tools and the use of other herbs in traditional Chinese medicine. The earliest (780 A.D.) written record on the subject, Cha Ching (tea book), pays homage to Shen Nong's discovery which it says he made when a gust of wind blew some tea leaves into a kettle of boiling water (Yu, 1974).
A competing legend started in India and followed the spread of Buddhism from India to China, Japan, and Southeast Asia. The British East India Company later advanced this legend as a part of its marketing strategy to weaken China's competitive advantage in global tea markets. It claims that tea was first grown in India and that Prince Siddhartha Gautama, Buddhism's founder, brought it to China. Tea was supposed to be a divine creation of the Buddha. The Prince was said to have torn off his eyelids and thrown them to the ground because he fell asleep despite his vow to remain awake during his pilgrimage through China. (There is no evidence he ever went to China). Supposedly, the eyelids took root and germinated into tea plants that sprouted leaves with an eyelid shape. All Siddhartha's fatigue was said to have vanished when he chewed the leaves of this plant.
In fact, the habit of chewing tea leaves was long established by the time of this alleged discovery (Evans, 1992). Evans also speculates, based on archeological evidence presented by Jelinek (1978), that the prehistoric people, Homo erectus pekinensis, were consumers of both boiling water and leaves, including tea leaves from wild forest plants, more than 500,000 years before tea legends became available for public consumption (Jelinek, 1978).
Today, both China and India (and possibly Burma and Thailand) share the distinction of tea's birthplace. Botanic evidence for this assertion has been found in the forests of these countries. Only there have tea plants been found that appear to be the wild type source of present-day cultivars. Although genuine wild type plants may no longer exist in these regions, previous explorations have determined that wild tea plants once grew from Nepal north and eastward to Formosa, the Liu-Kiu Islands, and southern Japan. Semi-wild species have been sighted from time to time in areas near the Assam-Burma border and in Indonesia, but they are believed to be tea left by migratory tea-drinking people (Kingdon-Ward, 1950).
Tea was introduced in the West by Turkish traders of the 6th century who apparently bartered for it at the Mongolian border. Then the Chinese of the Song Dynasty (960-1127 A.D.) realized tea's commercial value and actively exported it to Tibet. The tea traveled five miles a day by mule, yak, and on the backs of porters along 5,000-foot-high mountain passes. (One could compare 5,000-foot-high passes to stacks of 4 Empire State Buildings.) It is said that each man had to put opium behind his ears to deaden the pain of the 300-pound load strapped to his back (Weatherstone, 1992).
First the Dutch, then the British, began, then established the tea trade between China and Europe. Later, the British pioneered the cultivation and manufacture of tea in India and Ceylon where they introduced the plantation system. The Dutch did the same on Java and Sumatra. China's monopoly on this trade ended in the mid-1850s when its exports were surpassed by those of India and Ceylon. China's methods of cultivation on small plots could not compete with the output of Indian and Ceylonese plantations (Weatherstone, 1992).
Today tea is also grown in several African countries, Malaysia, Taiwan, Iran, Turkey (Turkish tea is no longer exported because it contains unacceptable amounts of radioactive contamination contributed by fallout from the Chernobyl nuclear power accident in 1986, although shipments are being made within Russia where contamination is considered to be at "acceptable" levels), Georgia and south Russia, Argentina, and even Brazil.
The first botanical classification of cultivated tea, made by Linnaeus in 1752, divided it into two species, Thea sinensis and Thea bohea. Later, when the number of petals was invalidated as a basis for this classification, Thea sinensis became the designation for the small-leaved China variety and Thea assamica the large-leaved Assam plant (Masters, 1844).
For a long time Thea and Camellia were considered to be separate genera, with cultivated tea plants included in the genus Thea and the non-tea Camellias in the genus Camellia. Nevertheless, confusion remained because major characteristics such as patina, leaf pose and pigmentation were, for all practical purposes, identical in both genera (Sharma & Venkataramani, 1974). Today, Thea and Camellia are considered to be synonymous (Wight, 1962) and the genus Camellia now belongs to the family Theaceae.
The most reliable diagnostic criteria for distinguishing the three recognized varieties of cultivated tea are provided by floral morphology: variation in the number of styles and the degree of their fusion; disposition of the stylar arm; and globular or pubescent ovary. For example, the styles are free for most of their length in the China variety (C. sinensis), fused for most of their length in the Assam variety (C. assamica), and remain free for about half their length in the Cambod race (C. assamica ssp. lasiocalyx). Growth habitat and leaf features continue to be used to distinguish between C. sinensis and C. assamica. Generally speaking the former is a small slow-growing shrub with small, narrow, serrate, dark green leaves, while the latter is a tall, quick-growing tree with large, horizontal, broad, light green leaves (Kitamura, 1950; Sealy, 1958).
Two other taxa, C. irrawadiensis and C. taliensis, are of interest because of their potential contribution to the genetic pool of tea. They, however, produce a liquor that lacks the quality of tea and are therefore not grown commercially. Other non-tea Camellia species, e. g. C. reticulata, C. sasanqua, and C. japonica, may have importance in understanding the evolution and interrelationships of Camellia species.
Because tea is easily cross-pollinated, all taxa freely interbreed to produce a cline (a gradual and more or less continual change between two extremes of a plant character occurring within the geographical range of a species) ranging from the China type plant to the Assam variety. Hybridization occurs so readily that the legitimacy of the three main tea taxa has been questioned (Visser, 1969). The possible contribution of other taxa to the tea genetic pool cannot be ruled out. Vegetative characters, e.g., internodal length, girth of bud, and leaf pose, are commonly used to group hybrids and relate them to the main taxa. Other anatomical differences, e.g., distribution and morphology of leaf sclereids (Barua, 1958) and leaf hair size and lumen length (Amma, 1986) have been shown to be useful. The potential for biochemical features such as polyphenol oxidase activity, individual polyphenols, amino acids, and chlorophyll contents has been realized but never fully utilized.
PHARMACOLOGY OF TEA CONSTITUENTS POLYPHENOLS
Upon ingestion, concentrations of tea polyphenols can be easily detected in blood, urine, and feces. Hence, polyphenols are absorbed and spread throughout the human or animal body. They probably exert their actions directly at the tissue and cellular level rather than have indirect intestinal effects (He & Kies, 1994).
The benefits associated with tea polyphenols, especially EGCG, are generally attributed to their antioxidant activity and their ability to scavenge free radical oxygen. But several other actions are suggested by studies of their role as chemopreventers.
Polyphenols are known to increase antioxidant and phase II enzyme activities in a variety of mouse organs, thus enhancing the overall chemopreventive effect of antioxidants in these organs (Khan, et al. 1992). One important phase II enzyme (UDP-glucuronosyl transferase), elevated in rat livers after treatment with green tea, may contribute to its anticancer effect by inactivating carcinogens and converting them into excretable form (Bu-Abbas, et al., 1995). Polyphenols also bind to cytochrome P450 in rat livers and indirectly block the activity of cytochrome P450-dependent enzymes. The cytochrome P450 superfamily contains sixty to several hundred oxidative enzymes that normally metabolize and detoxify numerous foreign chemicals in the liver. However, it has become apparent that genetic variants of these enzymes may sometimes function in an ambivalent manner, generating toxic or carcinogenic intermediates from the substances that they are supposedly detoxifying. Some of these en zymes convert procarcinogens to carcinogenic metabolites (Wang, et al., 1988; Mukhtar, et al., 1992). But green tea also stimulates the synthesis of certain forms of the P450 complex and could conceivably increase carcinogenic metabolites (Bu-Abbas, et al., 1994a).
In the test tube, the catechin gallates also selectively inhibit 5-à reductase, an enzyme responsible for the conversion of testosterone to 5-à dihydrotestosterone (Shutsung & Hiipakka, 1995). High levels of 5-à dihydrotestosterone are associated with benign prostate hyperplasia, prostate cancer, and male pattern baldness.
Many cancer-causing agents inhibit cell communication which may be an important mechanism of tumor development. The polyphenols, particularly the catechin gallates, may protect cells by enhancing gap junctional communication (Ruch, et al., 1989: Sigler & Ruch, 1993).
Another possible mechanism of action for tea polyphenols is suggested by the inhibition of tumor promoter binding to mouse skin. GTE (green tea extract) compounds might block by sealing receptors (Komori,et al., 1993). This mechanism might also explain why GTE blocks the uptake of nucleosides by tumors (a receptor-dependent mechanism) without affecting the uptake of receptor-independent cancer agents AraC and MTX (Zhen, et al., 1991). The report that tea extract inhibits the intestinal absorption of glucose and sodium in rats could be similarly explained (Kreydiyyeh, et al., 1994).
A different mode of preventive action by EGCG against carcinogenesis is suggested by Hayatsu, et al., (1992) who detects direct binding to certain carcinogens.
One study (Hu, et al., 1992) reports that EGCG stimulates B but not T cell proliferation and that the galloyl group is responsible for this enhancement. Confirmation of this important in vitro effect has not as yet appeared in the scientific literature.
The pharmacological effects of caffeine are an important reason for the popularity of tea Caffeine by far the most abundant methylxanthine in tea, may exert its behavioral and other effects through competitive antagonism at the adenosine-binding receptor. Caffeine levels, produced in humans by ingestion of a few cups of tea, are sufficient to antagonize adenosine's sympathetic nervous stimulation of the vascular system, heart, kidney, and adipose tissue (Rail, 1980). Although acute studies seem to suggest that caffeine is harmful to the cardiovascular system and worsens hypertension, the results of prolonged administration of caffeine do not support this contention (Robertson, et al., 1981). Caffeine does increase serum levels of non-esterified free fatty acids. Since these substances may cause cardiac arrhythmias, a mechanism is suggested for the rare association of caffeine ingestion and arrythmia.
Tea given to children (especially in Britain) is suspected of causing hyperactivity but no confirmation of that exists. In fact, 200-300 mg of caffeine per day has been used to treat hyperactivity (Marks, 1992).
Tea drinking has also been accused of promoting the formation of calcium oxalate-containing kidney stones because the caffeine induces calcium excretion and the tea itself is a source of oxalate. But no association has been found with either kidney or bladder stones (Marks, 1992).
Methylxanthines, particularly theophylline, are used in the treatment of asthma and bronchitis to relax the smooth muscle of the bronchi. However, the amounts of theophylline and theobromine ingested by drinking even large amounts of tea are too small to be pharmacologically significant. Their effects will not be considered here.
Tea has a long history as a medicinal plant and an even longer one as a beverage that ranks second only to water in worldwide popularity. In the West, this appeal stems from the stimulating and relaxing effects tea has on human physiology. In the East, that appeal is also based on cherished traditional beliefs in the health benefits of tea. Now, East meets West. The scientific basis for this belief is growing.
The animal and most recent epidemiological studies suggest that tea contains dietary factors which protect the consumer from the development of certain cancers, cardiovascular disease, some infectious diseases, and dental caries.
On the other hand, certain studies have concluded that tea may also have a negative or no effect on the growth of certain human, cancers. Why doesn't the animal data, which regularly shows health benefits, always agree with the human situation?
The problem may lie with inconsistencies between study designs. For example, studies have not always excluded or even identified the confounding variables that are linked to the tea drinking habit, the strength of that linkage to tea drinking, and its positive or negative impact on health independent of drinking tea. Clearly, better designed and carefully controlled epidemiological studies are needed; and they have been recommended (Mukhtar, et al., 1994). The results of the animal experiments are too compelling to be ignored.
Abe, Y., Umemura, S., Sugimoto, K., Hirawa, N., Kato. Y., Yokoyama, N., Yokoyama, T., Iwai, J., Ishii, M. 1995. Effect of green tea rich in gamma-aminobutyric acid on blood pressure of Dahl salt-sensitive rats, Am. J. Hypertens. 8:74-79.
Agarwal, R., Katiyar, S. K., Khan, S. G., Mukhtar, H. 1993. Protection against ultraviolet B radiation-induced effects in the skin of SKH-I hairless mice by a polyphenolic fraction isolated from green tea, Photochem. Photobiol. 58: 695-700.
Agudo, A., Gonzalez, C. A., Marcos. G., Sanz, M., Saigi, E., Verge, J., Boleda, M., Ortego, J. 1992. Consumption of alcohol, coffee, and tobacco and gastric cancer m Spain. Cancer Causes Control. 3:137-143.
Amma, S. 1986. Identification of tea clones Camellia sinensis (L.) Kuntze by pubescence on the undersurface of young leaves, in Development of New Technology for Identification and Classification of Tree Crops and Ornamentals (eds. K. Kitmura. T. Akihama, H. Kikimura. et al.). Fruit Research Station, Ministry of Agriculture, Forestry, and Fisheries, Japan, pp. 19-24.
Barnhart, R. K. 1988. in Dictionary of Etymology (ed. R. K. Barnhart), The H. W. Wilson Co., New York. NY, pp. 1118-1119.
Barua, D. N. 1958. Leaf sclerids in the taxonomy of Thea Camellias, I.Wilson's and related Camellias, Phytomorphology, 8, 257-264.
Bokuchava, M. A., Skobeleva, N. I. 1980. The biochemistry and technology of tea manufacture, Crit. Rev. Food Sci. Nutr. 12:303-370.
Brown. L. M., Swanson, C. A., Gridley, G., Swanson, G. M., Schoenberg, J. B., Greenberg, R. S., Silverman, D. T., Pottern. L. M., Hayes, R. B., Schwartz, A.G. 1995. Adenocarcinoma of the esophagus: Role of obesity and diet, J. Natl. Cancer Inst. 87:104-109.
Bu Abbas, A., Clifford, M. N., Ioannides, C, Walker, R. 1995, Stimulation of rat hepatic UDP-glucuronosyl transferase activity following treatment with green tea, Food Chem. Toxicol. 33:27-30.
Bu Abbas, A., Clifford, M. N., Walker, R., Ioannides, C. 1994a. Selective induction of rat hepatic CYPI and CYP4 proteins and of peroxisomal proliferation by green tea, Carcinogenesis. 15:2575-2579.
Bu Abbas, A., Clifford, M. N., Walker. R., Ioannides, C. 1994b. Marked antimutagenic potential of aqueous green tea extracts: Mechanism of action, Mutagenesis. 9:325-331.
Carr, M. K. V. 1972. The climatic requirements of the tea plant: A review, Experimental Agriculture. 8:1-14.
Chen, J. 1992. The effects of Chinese tea on the occurrence of esophageal tumors induced by N-nitrosomethylbenzylamine in rats. Prev. Med. 21:385-391.
Dexter, P. 1996. Personal communication to HerbalGram.
Dhar, G. M., Shah, G. N., Naheed, B. 1993. Epidemiological trend in the distribution of cancer in Kashmir Valley, J. Epidemiol. Community Health 47:290-292.
DiGiavanni. J. 1992. Multistage carcinogenesis in mouse skin, Pharmacol. Ther. 54: 63-128.
Eden, T. 1976. Tea, 3rd ed., Longman Group Limited London, pp. 177-178.
Elmets, C.A. 1991. Cutaneous photocarcinogenesis, in: Pharmacology of the Skin. [ed. H. Mukhtar] CRC Press, Boca Raton, FL, pp. 389-416.
Evans, J. C. 1992. Tea in China. New York: Greenwood Press, pp. 2-3, 7-8,
Franchesci, S., Barra, S., LaVecchia, C., Bidoli, E., Negri, E., Talmini, R. 1992. Risk factors for cancer of the tongue and the mouth. A case-control study from northern Italy, Cancer 70:2227-2233.
Fujita, Y., Yamane, T., Tanaka, M., Kuwata, K., Okuzumi, J., Takahashi, T., Fujiki, H., Okuda, T. 1989. Inhibitory effect of (-)-epigallocatechin gallate on carcinogenesis with N-ethyl-N'-nitro-N-nitrosoguanidine in mouse duodenum, Jpn. J. Cancer Res. 80:503-505.
Gao, Y. T., McLaughlin, J. K., Blot. W. J., Ji, B. T., Dai, Q., Fraumeni, J. F., Jr., 1994. Reduced risk of esophageal cancer associated with green tea consumption, J. Natl. Cancer Inst. 86:855-858.
Graham, H.N. 1992. Green tea composition, consumption, and polyphenol chemistry, Prev. Med. 21:334-350.
Hansson, L. E., Nyren, O., Bergstrom, R., Wolk, A., Lindgren, A., Baron, J., Adami, H. O. 1993. Diet and risk of gastric cancer. A population-based case-control study in Sweden, Int. J. Cancer 55:181-189.
Hayatsu. H., Inada, N., Kakutani, T., Arimoto, S., Negishi, T., Mort, K., Okuda, T., Sakata, I. 1992. Suppression of genotoxicity of carcinogens by (-)-epigallocatechin gallate, Prev. Med. 21:370-376.
He, Y. H., Kies, C. 1994. Green and black tea consumption by humans: Impact on polyphenol concentrations in feces, blood and urine. Plant Foods Hum. Nutr. 46:221-229.
Henry, J.P., Stephens-Larsen, P. 1984. Reduction of chronic psychosocial hypertension in mice by decaffeinated tea, Hypertension. 6:437-444.
Hertog, M. G., Feskens, E. J., Hollman, P. C., Katan, M. B., Kromhout, D. 1993. Dietary antioxidant flavonoids and risk of coronary heart disease: The Zutphen Elderly Study, Lancet. 342:1007-1011.
Hirose, M., Hoshiya, T., Akagi, K., Futakuchi, M., Ito, N. 1994. Inhibition of mammary gland carcinogenesis by green tea catechins and other naturally occurring antioxidants in female Sprague-Dawley rats pretreated with 7, 12-dimethylbenz[alpha]anthracene, Cancer Lett. 83:149-156.
Hirose, M., Hoshiya, T., Akagi, K., Takahashi, S., Hara, Y., Ito, N. 1993. Effects of green tea catechins in a rat multi-organ carcinogenesis model, Carcinogenesis 14:1549-1553.
Horiba, N., Maekawa. Y., Ito. M., Matsumoto, T., Nakamura, H. 1991. A pilot study of Japanese green tea as a medicament: Antibacterial and bactericidal effects, J. Endod. 17:122-124.
Hu, Z. Q., Toda, M., Okubo, S., Hara, Y., Shimamura, T 1992. Mitogenic activity of (-) epigallocatechin gallate on B-cells and investigation of its structure-function relationship, Int. J. Immunopharmacol. 14:1399-1407.
Huang, M-.T. Ho, C. T., Wang, Z. Y., Ferraro, T, Finnegan-Olive, T., Lou, Y. R., Mitchell, J. M., Laskin, J. D., Newmark, D., Yang, C. S., Connery, A. H. 1992. Inhibitory effect of topical application of a green tea polyphenol fraction on tumor initiation and promotion in mouse skin, Carcinogenesis. 13:947-954.
IARC Monographs on the evaluation of the carcinogenic risk to humans: coffee, tea, mate, methylxanthines, and methylglyoxal. 1991. International Agency for Research on Cancer Working Group, Vol. 51.
Ikigai, H., Nakae, T., Hara, Y., Shimamura, T. 1993. Bactericidal catechins damage the lipid bilayer, Biochim. Biophys. Acta. 1147:132-136.
Imai, K., Nakachi, K. 1995. Cross sectional study of effects of drinking green tea on cardiovascular and liver diseases, Brit. Med. J. 310:693-696.
Jelinek, J., ed., 1978. Illustrated Encyclopedia of Prehistoric Man (Paris:Grund), Chapter 1.
Katiyar, S. K., Agarwal, R., Mukhtar, H. 1993a. Inhibition of stage I and stage II skin tumor promotion in SENCAR mice by a polyphenolic fraction isolated from green tea: Inhibition depends on the duration of polyphenol treatment, Carcinogenesis 14:2641-2643.
Katiyar, S. K., Agarwal, R., Mukhtar, H. 1993b. Protection against malignant conversion of chemically induced benign skin papillomas to squamous cell carcinomas in SENCAR mice by a polyphenolic fraction isolated from green tea, Cancer Res. 53:5409-5412.
Katiyar, S. K., Agarwal, R., Mukhtar, H. 1994. Inhibition of spontaneous and photo-enhanced lipid peroxidation in mouse epidermal microsomes by epicatechin derivatives from green tea, Cancer Lett. 79:61-66.
Katiyar, S. K., Agarwal, R., Wang, Z. Y., Bhatia, A. K., Mukhtar, H. 1992a. (-)-Epigallocatechin-3- gallate in Camellia sinensis leaves from the Himalayan region of Sikkim: Inhibitory, effects against biochemical events and tumor initiation in SENCAR mouse skin. Nutr. Cancer 18:73-83.
Katiyar, S. K., Agarwal, R., Wood, G. S., Mukhtar, H. 1992b. Inhibition of 12-O-tetradecanoylphorbol-13-acetate-caused tumor promotion in 7, 12-dimethylbenz[a]anthracene-initiated SENCAR mouse skin by a polyphenolic fraction isolated from green tea, Cancer Res 52:6890-6897.
Katiyar, S. K., Agarwal, R., Zaim, M. T., Mukhtar, H. 1993c. Protection against N-nitrosodiethylamine and benzo[a]pyrene-induced forestomach and lung tumorigenesis in A/J mice by green tea, Carcinogenesis. 14:849-855.
Keating, B., Razor, M. 1996. Tea is hot: Diverse factors driving the burgeoning U.S. tea industry, HerbalGram 35:59.
Khan, S. G., Katiyar, S. K., Agarwal, R., Mukhtar, H. 1992. Enhancement of antioxidant and phase II enzymes by oral feeding of green tea polyphenols in drinking water to SKH-1 hairless mice: Possible role in cancer chemoprevention, Cancer Res. 52:4050-4052.
Kingdon-Ward, F. 1950. Does wild tea exist? Nature 165:297-99.
Kitamura, S. 1950. Acta phytotax and Geobot, Kyoto, 14:56.
Komori, A., Yatsunami, J., Okabe, S., Abe, S., Hara, K., Suganuma, M., Kim, S. J., Fujiki, H. 1993. Anticarcinogenic activity of green tea polyphenols, Jpn. J. Clin. Oncol. 23:186-190.
Kono, S., Shinchi, K., Ikeda, N., Yanai, F, Imanishi, K. 1992. Green tea consumption and serum lipid profiles: A cross-sectional study in Northern Kyoshu, Japan, Prev. Med. 21 526-531.
Kono, S., Shinchi, K., Ikeda, N., Yanai, F., Imanishi, K. 1991. Physical activity, dietary habits and adenomatous polyps of the sigmoid colon: A study of self-defense officials in Japan, J. Clin. Epidemiol. 44:1255-1261.
Kreydiyyeh, S. I., Abdel-Hasan-Baydoun, E., Churukian, Z. M. 1994. Tea extract inhibits intestinal absorption of glucose and sodium in rats, Comp. Biochem. Physiol. Pharmacol. Toxicol. Endocrinol. 108:359-365.
Kumar, R., Mende, P., Wacker, C. D., Spiegelhalder,B., Preussmann, R., Siddiqi, M. 1992. Caffeine-derived N-nitroso compounds -- I: Nitrosatable precursors from caffeine and their potential relevance in the etiology of oesophageal and gastric cancers in Kashmir, India, Carcinogenesis. 13:2179-2982.
Makimura, M., Hirasawa, M., Kobayashi, K., Indo, J., Sakanaka, S., Taguchi, T., Otake, S. 1993. Inhibitory effect of tea catechins on collagenase activity, J. Periodontol. 64 630-636.
Marks, V. 1992. Physiological and clinical effects of tea, in Tea: Cultivation to Consumption (eds. K. C. Willson and M. N. Clifford), Chapman & Hall, New York, pp. 707-734.
Masters, J. W. 1844. The Assam tea plant compared with tea plant in China, Journal of Agri-Horticultural Society India.
Miura, S., Watanabe, J., Sano, M., Tomita, T., Osawa, T., Hara, Y., Tomita, I. 1995. Effects of various antioxidants on the Cu (2+)-mediated oxidative modification of low density lipoprotein, Biol. Pharm. Bull. 18:1-4.
Mukhtar, H., Katiyar, S. K., Agarwal, R. 1994. Green tea and skin -- anticarcinogenic effects, J. Invest. Dermatol. 102:3-7.
Mukhtar, H., Wang, Z. Y., Katiyar, S. K., Agarwal, R. 1992. Tea components: Antimutagenic and anticarcinogenic effects, Prev. Med. 21:351-360.
Nakane, H., Ono, K. 1990. Differential inhibitory effects of some catechin derivatives on the activities of human immunodeficiency virus reverse transcriptase and cellular deoxyribonucleic and ribonucleic acid polymerases, Biochemistry. 29:2841-2845.
Nakayama, M., Suzuki, K., Toda, M., Okubo, S., Hara, Y., Shimamura, T. 1993. Inhibition of the infectivity of influenza virus by tea polyphenols, Antiviral Res. 21:289-299.
Narisawa, T., Fukaura, Y. 1993. A very low dose of green tea polyphenols in drinking water prevents N-methyl-N-nitrosourea-induced colon carcinogenesis in F344 rats, Jpn. J. Cancer Res. 84:1007-1009.
Otake, S., Makimura, M., Kuroki, T., Nishihara, Y., Hirasawa, M. 1991. Anticaries effects of polyphenolic compounds from Japanese green tea, Caries Res. 25:438-443.
Othieno, C. O. 1992. Climate, weather and the yield of tea, in Tea: Cultivation to Consumption (eds. K. C. Willson and M. N. Clifford) Chapman & Hall, New York, pp. 87-135.
Rall, T. W. 1980. The xanthines, in The Pharmacological Basis of Therapeutics, (eds. A. G. Gilman, L. S. Goodman, A. Gilman), Macmillan, New York, pp. 592-607.
Robertson, D., Wade, D., Workman, R, et al. 1981. Tolerance to the humoral and hemodynamic effects of caffeine in man, J. Clin, Invest, 67:1111-1117.
Ruch, R. J., Cheng, S. J., Klaunig, J. E. 1989. Prevention of cytotoxicity and inhibition of intercellular communication by antioxidant catechins isolated from Chinese green tea, Carcinogenesis. 10:1003-1008.
Ryu, E. 1982. Prophylactic effect of tea on pathogenic microorganism infections to humans and animals, Int. J. Zoonoses. 9:126-131.
Sadakata, S., Fukao, A., Hisamichi, S. 1992. Mortality among female practitioners of Chanyou (Japanese "tea-ceremony"), Tohoku J. Exp. Med. 166:475-477.
Sanderson, G.W. 1963. The chloroform test -- A study of its suitability as a means of rapidly evaluating fermenting properties of clones, Tea Quarterly. 34:193-196.
Sasaki, Y. F., Matsumoto, K., Imanishi, H., Watanabe, M., Ohta, T., Shirasu, Y., Tutikawa, K. 1990. In vivo anticlastogenic and antimutagenic effects of tannic acid in mice, Mutat. Res. 244:43-47.
Sasaki, Y. F., Yamada, H., Shimoi, K., Kator, K., Kinae, N. 1993. The aclastogen-suppressing effects of green tea. Po-lei tea and Rooibos tea in CHO cells and mice, Mutat. Res. 286:221-232.
Sato, Y., Nakatsuka, H., Watanabe, T., Hisamichi, S., Shimizu, H., Fujisaku, S., Ichinowatari. Y., Ida, Y., Suda, S., Kato, K., et al. 1989. Possible contribution of green tea drinking habits to the prevention of stroke, Tohoku. J. Exp, Med. 157:337-343
Schwarz, B., Bischof, H. P., Kunze, M. 1994. Coffee, tea and lifestyle. Prev. Med. 23: 377-384.
Sealy, J. 1958. A Revision of the Genus Camellia, Royal Horticultural Society, London.
Sharma, V. S., Venkataramani, K. S. 1974. The Tea Complex. I. Taxonomy of tea clones, Proceedings, Indian Academy of Sciences, 53B:178-187.
Shetty, M., Subbannayya, K., Shivananda, P.G. 1994. Antibacterial activity of tea (Camellia sinensis) and coffee (Coffee arabica) with special reference to Sahnonella typhimurium. J. Commun, Dis. 26:147-150.
Shibata, A., Mack, T. M., Paganini-Hill, A., Ross, R. K., Henderson, B. E. 1994. A prospective study of pancreatic cancer in the elderly, Int. J. Cancer 58: 46-49.
Shouyi, B. ed., 1982. An Outline History of China (Beijing: Foreign Languages Press. 1982), pp. 55.
Shutsung, L., Hiipakka, R.A. 1995. Selective inhibition of steroid 5a-reductase isoenzymes by tea epicatechin-3-gallate and epigallocatechin-3-gallate, Biochem. Biophys. Res. Comm. 214:833-838.
Sigler, K., Ruch, R. J. 1993. Enhancement of gap junctional intercellular communication in tumor promoter-treated cells by components of green tea, Cancer Lett. 69:15-19.
Spillane, M. Personal communication to HerbalGram. May 16, 1996.
Steinberg. D., Parthasarathy, S., Carew, T. E., Khoo, J. C., Witztum, J. L. 1989. Modifications of low-density lipoprotein that increase its atherogenicity, N. Engl. J. Med. 320:915-924.
Tanaka, S. 1973. The Tea Ceremony. Kodansha International Ltd.: Tokyo.
Taniguchi, S., Fujiki, H., Kobayashi. H., Go, H., Miyado, K., Sadano, H., Shimokawa, R. 1992. Effect of (-)-epigallocatechin gallate, the main constituent of green tea, on lung metastasis with mouse B16 melanoma cell lines. Cancer Lett. 65:51-54.
Tanizawa, H., Toda, S., Sazuka, Y., Taniyama, T, Hayashi, T., Arichi, S., Takino, Y. 1984. Natural antioxidants. I. Antioxidant components of tea leaf (Thea sinensis). Chem. Pharm. Bull. 32:2011-2014.
Uchida, S., Edamatsu, R., Hiramatsu, M., Mori, A., Nonaka, G., Nishioka, I., Niwa, M., Ozaki, M. 1987. Condensed tannins scavenge oxygen free radicals. Med Sci. Res. 15: 831-832.
Uchida, S., Ozaki, M., Suzuki, K., Shikita, M. 1992. Radioprotective effects of (-)-epigallocatechin-3-O-gallate (green tea tannin) in mice, Life Sci. 50:147-152.
Visser, T. 1969. Tea Camellia sinensis (L.) O. Kuntz, in Outlines of Perennial Crop Breeding in the Tropics (ed. F. P. Ferwada and F. Wit], H. Veenan and Zonen, Wageningen, pp. 459-493.
Wang, Z. Y., Cheng, S. J., Zhou, Z. C., Athar, M., Khan, W. A., Bickers, D. R., Mukhtar, H. 1989. Antimutagenic activity of green tea polyphenols, Mutat. Res. 223:273-285.
Wang, Z. Y., Das, M., Bickers, D. R., Mukhtar, H. 1988. Interaction of epicatechins derived from green tea with rat hepatic cytochrome P-450, Drug Metab. Dispos. Biol. Fate Chem. 16:98-103.
Wang, Z.Y., Hong, J. Y., Huang, M. T, Reuhl, K. R., Conney, A. H., Yang, C. S. 1992c. Inhibition of N-nitrosodiethylamine-and 4-(methylnitrosoamin)-1-(3-pyridyl)-1-butanone-induced tumorigenesis in A/J mice by green tea and black tea, Cancer Res. 52: 1943-1947.
Wang, Z. Y., Huang, M. T., Ho, C. T., Chang, R., Ma, W., Ferraro, T., Reuhl, K. R., Yang, C. S., Conney, A. H. 1992a. Inhibitory effect of green tea on the growth of established skin papillomas in mice, Cancer Res. 52:6657-6665.
Wang, Z. Y., Huang, M. T, Ferraro, T, Wong, C. Q., Lou, Y. R., Reuhl, K., Iatropoulos, M., Yang, C. S., Conney, A. H. 1992b. Inhibitory effect of green tea in the drinking water on tumorigenesis by ultraviolet light and 12-O-tetradecanoylphorbol-13-acetate in the skin of SKH-1 mice, Cancer Res. 52:1162-1170.
Wang, Z. Y., Huang, M. T., Lou, Y. R., Xie, J. G., Reuhl, K. R., Newmark, H. L., Ho, C. T., Yang, C. S., Conney, A. H. 1994. Inhibitory effects of black tea, green tea, decaffeinated black tea, and decaffeinated green tea on ultraviolet B light-induced skin carcinogenesis in 7,12-dimethylbenz[a]anthracene-initiated SKH-1 mice, Cancer Res. 54:3428-3435.
Weatherstone, J. 1992. Historical Introduction, in Tea: Cultivation to Consumption [eds. K. C. Willson and M. N. Clifford] Chapman and Hall, New York, pp. 1-23.
Weisburger, J. H., Nagao, M., Wakabayashi, K., Oguri, A. 1994. Prevention of heterocyclicamine formation by tea and tea polyphenols, Cancer Lett. 83:143-147.
Wight, W., Barua, D. N. 1954. Morphological basis of quality in tea. Nature 173:630-631.
Wight, W. 1958. The agrotype concept in tea taxonomy, Nature 181, 893-895.
Wight, W. 1962. Tea classification revised, Current Science, 31:298-9.
Willson, K.C. 1992a Propagation, in Tea: Cultivation to Consumption (eds. K. C. Willson and M. N. Clifford) Chapman & Hall, New York, pp. 209-217.
Willson, K.C. 1992b. Field operations: 2, in Tea: Cultivation to Consumption (eds. K. C. Willson and M. N. Clifford) Chapman & Hall, New York, pp. 227-265.
Xu, Y., Ho, C. T., Amin, S. G., Ha