Black tea,green tea,and tea polyphenols

Previous studies have shown that tea consumption can impair trace element metabolism, particularly iron status, and increase the risk of anemia in humans and animals. More recently, however, evidence has been accumulating to show that, in animals, consumption of green tea or its polyphenols is associated with a reduction of the incidence and severity of a variety of experimentally induced cancers. In this study we have monitored the growth, trace element status, including hematological parameters of weanling rats given either (1) water, (2) 1% black tea, (3) 1% green, tea, or (4) 0.2% crude green tea extract as their sole drinking fluid while consuming diets containing either adequate or low amounts of iron. With the exception of manaanese, none of the trace elements studied (iron, copper, zinc, and manganese) or the hematological indices measured were affected by the type of beverage supplied, even though the polyphenol extract was shown to chelate metals in vitro and all the animals fed the low iron diet were shown to be anemic. There appeared to be an effect of black and green teas on manganese balance in, both the first and last weeks of the study. A lower level of brain managanese was associated with green tea consumption, and a higher level of this element in the kidneys of animals fed black tea. The results demonstrate that both black and green teas and a green tea polyphenol extract do not represent a risk to animals consuming the beverages as their sole fluid intake with respect to iron availability, although the interactions with manganese deserve further study.     

Ultrastructural changes in tea leaves during 'orthodox' black tea manufacture

Changes in fine structure of upper epidermal and palisade cells of fresh, withered, rolled, ‘fermented’ and ‘fired’ tea leaves have been studied. In the fresh immature leaves, the polyphenols are located mainly in the vacuoles of the first two to three layers of upper palisade cells. Loss of water during withering causes slight disorganization in the fine structure of the organelles. Rolling causes extensive disorganization of the organelles, membranes and cell walls. The chloroplast membranes, which are rich in lipoproteins, rupture and parts of it vesiculate. These controlled and defined changes in fine structure leading to cell death, characterized by cleavage of cell walls in certain areas, rupture of the membranes, organelles and their inclusions, followed by‘cramped plasmolysis’ of cellular contents, throw more light on the biochemical changes that take place during tea manufacture.     

Lipid degradation during manufacture of black tea

About 85% of the fatty acids liberated during the manufacture of black tea can be attributed to autolysis of 4 major polar lipid classes in tea leaf tissue, phosphatidylcholine, monogalactosyldiglyceride, digalactosyldiglyceride and phosphatidylethanolamine. Linolenic, linoleic and palmitic acids are the principal fatty acids released from these lipids and they all undergo further degradation. Linolenic acid (60% of fatty acids released) is derived mainly from galactolipids and thus the upper limit of release is dependent on the chloroplast maturity and content of the leaf tissues. Lipid breakdown is complete after 2 hr fermentation and, as there appears to be no accumulation of long chain fatty acid intermediates, it is probable that volatile production has also ceased at this time.     

Black tea represents a major source of dietary phenolics among regular tea drinkers

The phenolic composition and antioxidant activities [TEAC, ORAC, FRAP] of consumer brews (1 tea bag in 230 ml for 1 min) of seven different brands of black tea from the British market were investigated. The main phenolic compounds identified were epigallocatechin gallate, four theaflavins, as well as epicatechin gallate, theogallin (tentative assignment), quercetin-3-rutinoside and 4-caffeoyl quinic acid. Thearubigins represented an estimated 75-82% of the total phenolics. Further, polyphenol fractions were in decreasing order theaflavins, flavan-3-ols, flavonols, gallic acids and hydroxycinnamates. On average, a cup of a consumer brew of black tea is providing polyphenols at the level of 262 mg GAE/serving, of which 65 mg were assigned to individual polyphenols. The antioxidant activity of black tea preparations is higher than that of most reported dietary agents on a daily basis. Correlations were observed between the antioxidant activities and the sum of all quantified polyphenols by HPLC analysis as well as with the total phenolics. Treatment of the black tea brew with simulated gastric juice resulted in a significant increase of the identified theaflavins implying a partial cleavage of thearubigins in the environment of the gastric lumen. Therefore, black tea can be considered to be a rich source of polyphenols and/or antioxidants.     

Production of volatiles by degradation of lipids during manufacture of black tea

During manufacture of black tea, lipids are degraded to volatile constituents. Cis-3-hexenal was present in appreciable amounts in the various parts of fresh shoots and decreased in the second leaves during manufacture. There was a simultaneous increase in trans-2-hexenal. Linalol and methyl salicylate also increased appreciably during rolling and fermentation. Most of the volatiles were lost during the firing process. The above trend was borne out by the ‘potential’ of the leaves for the production of volatiles as indicated by the increased amounts of volatiles produced by homogenizing the tissue in water against controls homogenized in 0.1 N acid. The C₆-aldehydes present in the headspace of withered shoots increased significantly following mechanical damage. The major fatty acids of the lipids in the various parts of the shoots were linolenic, linoleic, palmitic, oleic and stearic acids. The ratio of linoleic to linolenic acid in the stems was much higher than that of the leaves or buds and this was reflected in its higher 'potential for formation of hexanal. During withering and rolling of the second leaves, the unsaturated fatty acids showed substantial losses compared with the saturated acids. It is suggested that the enzymic breakdown of membrane lipids initiate the formation of volatile carbonyl compounds which are partly responsible for the flavour of black tea.     

Black and green tea and heart disease: a review

Tea is the second most consumed beverage around the world behind water. Epidemiological evidence points to both green and black tea consumption being protective with respect to heart disease. However, epidemiological evidence does not prove cause and effect and is potentially flawed by confounding variables. The recent evidence with respect to teas' beneficial effects from in vitro and in vivo studies in both animals and humans will be covered in this review. The comparative benefits of green vs. black tea will be considered. Articles published through December, 1999 will be included.     

Black tea extract supplementation decreases oxidative damage in Jurkat T cells

The purpose of this study was to investigate the protective effect of black tea (BT) extract against induced oxidative damage in Jurkat T-cell line. Cells supplemented with 10 or 25 mg/L BT were subjected to oxidation with ferrous ions. Malondialdehyde (MDA) production as marker of lipid peroxidation, DNA single strand breaks as marker of DNA damage, and modification of the antioxidant enzyme activity, glutathione peroxidase (GPX) were measured. Results show the efficacy of BT polyphenols to decrease DNA oxidative damage and to affect GPX activity (P<0.05), while no effect was shown on MDA production. The succeeding investigation of the activity of caffeine and epigallocatechin gallate demonstrated their antioxidant potential with respect to the cellular markers evaluated. In conclusion, this study supports the protective effect of BT against ferrous ions induced oxidative damage to DNA and the ability of BT to affect the enzyme antioxidant system of Jurkat cells.     

Black tea theaflavins suppress dioxin-induced transformation of the aryl hydrocarbon receptor

Dioxins cause various adverse effects through transformation of aryl hydrocarbon receptor (AhR). In this study, we investigated whether black tea extract and its components, theaflavins, suppress AhR transformation in vitro. First, we confirmed that black tea extract strongly suppressed AhR transformation compared to green and oolong tea, although the catechin contents did not change significantly among the extracts. Then we isolated four theaflavins as active compounds from black tea leaves. They suppressed 1 nM 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced AhR transformation in a dose-dependent manner. The IC(50) values of theaflavin, theaflavin-3-gallate, theaflavin-3'-gallate, and theaflavin-3,3'-digallate (Tfdg) were 4.5, 2.3, 2.2, and 0.7 muM, respectively. The suppressive effect of Tfdg was observed not only by pre-treatment but also by post-treatment. This suggests that theaflavins inhibit the binding of TCDD to the AhR and also the binding of the transformed AhR to the specific DNA-binding site as putative mechanisms.     

Black tea extract suppresses transformation of aryl hydrocarbon receptor induced by dioxin

Dioxins cause various adverse effects through binding to an aryl hydrocarbon receptor (AhR) and transformation of the receptor. In this study, we investigated whether black tea extract suppresses AhR transformation. Dried black tea leaves were extracted with 75% ethanol, and the extract was pretreated to the rat liver cytosol fraction 10 min prior to addition of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Transformed AhR was detected by electrophoretic gel mobility shift assay. Black tea extract suppressed AhR transformation in a dose-dependent manner, and the IC50 value against 1 nM TCDD-induced AhR transformation was 8.9 microg/ml. The result suggests that intake of black tea has a potential to suppress the AhR transformation, leading protection from dioxin toxicity.     

Black tea increases the resistance of human plasma to lipid peroxidation in vitro, but not ex vivo.

A number of in vitro studies have shown that polyphenols and flavonoids in tea exert significant antioxidant activity. However, epidemiologic and experimental studies have produced conflicting results. The purpose of the present study was to compare the antioxidant activity of black tea in vitro with that ex vivo. Black tea polyphenols (BTP), black tea extract (BTE), or their major polyphenolic antioxidant constituent, epigallocatechin gallate (EGCG), were added to human plasma and lipid peroxidation was induced by the water-soluble radical generator 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH). Following a lag phase, lipid peroxidation was initiated and occurred at a rate that was lowered in a dose-dependent manner by BTP. Similarly, EGCG and BTE added to plasma in vitro strongly inhibited AAPH-induced lipid peroxidation. The lag phase preceding detectable lipid peroxidation was due to the antioxidant activity of endogenous ascorbate, which was more effective at inhibiting lipid peroxidation than the tea polyphenols and was not spared by these compounds. In contrast, when eight healthy volunteers consumed the equivalent of six cups of black tea, the resistance of their plasma to lipid peroxidation ex vivo did not increase over the next 3 h. These data suggest that, despite antioxidant efficacy in vitro, black tea does not protect plasma from lipid peroxidation in vivo. The striking discrepancy between the in vitro and ex vivo data is most likely explained by the insufficient bioavailability of tea polyphenols in humans.     

Black tea is a powerful chemopreventor of reactive oxygen and nitrogen species: comparison with its individual catechin constituents and green tea

Production of black tea [BT] results in biotransformation of catechins of green tea [GT] to theaflavins and thearubigins. BT was found to be more efficient than GT and its individual catechin constituents in proportionate amounts in abrogating production of NO and O2(-) in activated murine peritoneal macrophages. In a reconstitution system of BT that is free of all catechins, stepwise addition of catechins showed that though all the constituents contributed to the overall effect of BT, theaflavin was the most powerful in abrogating NO production. RT-PCR analysis also showed theaflavin to be the most important constituent in down-regulating synthesis of iNOS. Clearly, BT containing theaflavin is an excellent chemopreventor against reactive oxygen and nitrogen species.     

Black tea affects obesity by reducing nutrient intake and activating AMP-activated protein kinase in mice

The effects of certain tea components on the prevention of obesity in humans have been reported recently. However, whether Yinghong NO. 9 black tea consumption has beneficial effects on obesity are not known. Here, we obtained a Yinghong NO. 9 black tea infusion (Y9 BTI) and examined the anti-obesity effects of its oral administration. ICR mice were fed a standard diet supplemented with Y9 BTI at 0.5, 1.0, or 2.0 g/kg body weight for two weeks, and the body weight were recorded. HE staining was used to evaluate the effect of Y9 BTI on mice liver. Western blot analysis was used to detect the expression levels of related proteins in the mice liver and adipose. We found that the body weights of the mice in the control group were significantly higher than those of the mice in the middle and high dose groups. The results of western blot showed that Y9 BTI up-regulated the expression of liver kinase B1 (LKB1) and adenosine monophosphate-activated protein kinase (AMPK) and also increased in AMPK phosphorylation (p-AMPK) and LKB1 phosphorylation (p-LKB1). Y9 BTI significantly down-regulated Fas Cell Surface Death Receptor(FAS) and activated the phosphorylation of acetyl-CoA carboxylase (ACC). Furthermore, Y9 BTI (2.0 g/kg BW) down-regulated the expression of three factors (IL-1β, Cox-2, and iNOS). Altogether, Y9 BTI supplementation reduced the feed intake of mice and may prevent obesity by inhibiting lipid absorption. These results suggest that Y9 BTI may regulate adipogenic processes through the LKB1/AMPK pathway.