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Green tea and skin--anticarcinogenic effects.

Because of its special aroma, green tea is a popular beverage consumed by some human populations worldwide. In recent years, many laboratory studies have shown that in a variety of animal tumor bioassay systems the administration of green tea, specifically the polyphenolic fraction isolated from green tea leaves (green tea polyphenols), affords protection against cancer induction. In mouse skin tumor bioassay systems, topical application of green tea polyphenols to skin has been shown to result in protection against a) 3-methylcholanthrene-induced skin tumorigenicity, b) 7,12-dimethylbenz(a)anthracene (DMBA)-induced skin tumor initiation, c) 12-O-tetradecanoylphorbol-13-acetate and other tumor promoters caused tumor promotion in DMBA-initiated skin, and d) benzoyl peroxide- and 4-nitroquinoline N-oxide caused enhanced malignant progression of nonmalignant lesions. Green tea extract has also been shown to cause partial regression of established skin papillomas in mouse. Similarly, chronic oral feeding of green tea polyphenols or water extract of green tea has also been shown to result in the protection against both chemical carcinogen- and ultraviolet B radiation-induced skin tumorigenicity. Collectively these data suggest that green tea possesses significant chemopreventive effect against each stage of carcinogenesis, and that it may be useful against inflammatory responses associated with the exposure of skin to chemical tumor promoters as well as to solar radiation. Available data regarding the mechanism by which green tea affords these diversified effects is discussed.

9,10-Dimethyl-1,2-benzanthracene↗

Green tea polyphenols induce apoptosis in vitro in peripheral blood T lymphocytes of adult T-cell leukemia patients.

Green tea polyphenols (TEA) are known to exhibit antioxidative activity as well as tumor-suppressing activity. In order to examine the tumor-suppressing activity of TEA against adult T-cell leukemia (ATL), we cultivated peripheral blood T lymphocytes of ATL patients (ATL PBLs), an HTLV-I-infected T-cell line (KODV) and healthy controls (normal PBLs) for 3 days in the presence of TEA and its main constituent, epigallocatechin-3-gallate (EGCg), to measure cell proliferation and apoptosis, and to quantitate mRNAs of HTLV-I pX and beta-actin genes of the cultured cells. Growth of ATL PBLs was significantly inhibited by 9-27 microg/ml of TEA and EGCg, in contrast to minimal growth inhibition of T cells of normal PBLs. Inhibition of KODV was intermediate between ATL PBLs and normal PBLs. The ATL PBLs and KODV treated with 27 microg/ml of either TEA or EGCg induced apoptotic DNA fragmentation, producing terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells, while the normal PBLs treated with the same concentration of TEA or EGCg produced a negligibly small number of TUNEL-positive cells, in which apoptotic DNA fragmentation was not detectable. Expression of HTLV-I pX mRNA was suppressed more than 90% in ATL PBLs by treatment with 3-27 microg/ml of either TEA or EGCg, while expression of beta-actin mRNA was much less suppressed by treatment with the same concentration of TEA or EGCg. These results indicate that TEA and EGCg inhibit growth of ATL PBLs, as well as HTLV-I-infected T-cells, by suppressing HTLV-I pX gene expression and inducing apoptotic cell death.

Adult↗

[Protective activity of tea and catechins against Bordetella pertussis].

We examined the bactericidal activity of tea and catechins against Bordetella pertussis. Green tea, black tea and coffee showed marked bactericidal activity at their concentrations in beverages, while pu-erh tea killed the bacteria in a moderate way. (-) Epigallocatechin gallate (EGCg) and theaflavin digallate (TF3) showed also marked bactericidal activity. Green tea and black tea also effectively blocked the adhesion of B. pertussis to HeLa and CHO cells, whereas ECGg and TF3 could not. EGCg and TF3 markedly inactivated leuco-lymphocytosis promoting activity of pertussis toxin. Black tea showed slight but significant inactivation of the activity, whereas green tea showed no inactivation. These results suggest that green tea, black tea, EGCg and TF3 might act as prophylactic agents against pertussis infection.

Animals↗

Inhibition of carcinogenesis by tea.

Tea has received a great deal of attention because tea polyphenols are strong antioxidants, and tea preparations have inhibitory activity against tumorigenesis. The bioavailability and biotransformation of tea polyphenols, however, are key factors limiting these activities in vivo. The inhibition of tumorigenesis by green or black tea preparations has been demonstrated in animal models on different organ sites such as skin, lung, oral cavity, esophagus, forestomach, stomach, small intestine, colon, pancreas, and mammary gland. Epidemiological studies, however, have not yielded clear conclusions concerning the protective effects of tea consumption against cancer formation in humans. The discrepancy between the results from humans and animal models could be due to 1) the much higher doses of tea used in animals in comparison to human consumption, 2) the differences in causative factors between the cancers in humans and animals, and 3) confounding factors limiting the power of epidemiological studies to detect an effect. It is possible that tea may be only effective against specific types of cancer caused by certain etiological factors. Many mechanisms have been proposed for the inhibition of carcinogenesis by tea, including the modulation of signal transduction pathways that leads to the inhibition of cell proliferation and transformation, induction of apoptosis of preneoplastic and neoplastic cells, as well as inhibition of tumor invasion and angiogenesis. These mechanisms need to be evaluated and verified in animal models or humans in order to gain more understanding on the effect of tea consumption on human cancer.

Angiogenesis Inhibitors↗

Effect of different levels of an ascorbic acid and tea mixture on nonheme iron absorption from a typical Tunisian meal fed to healthy rats.

The aim of our study was to evaluate the bioavailability of iron from a typical Tunisian meal 'couscous' provided to healthy rats with or without appropriate mixtures of tea plus ascorbic acid and to search for the optimal amount of ascorbic acid able to overcome the inhibitory effect of tea prepared under realistic Tunisian circumstances. Our findings show that a tea decoction (100 mg/ml) reduced nonheme iron absorption from couscous by 50% (16.5 vs. 33.1%; p < 0.01). In contrast, administration of 20 mg ascorbic acid increased nonheme iron absorption from couscous by more than 100% (66.8 vs. 33.1%; p < 0.001). Administration of ascorbic acid (20 mg) in a tea decoction (100 mg/ml) completely counteracted the inhibiting effect of tea and significantly improved the nonheme iron absorption from couscous (34 vs. 33% in the control group; NS). The same effect was shown when 10 mg ascorbic acid was added to the tea decoction; however, 5 mg ascorbic acid was not able to overcome the inhibitory effect of tea on nonheme iron absorption from couscous (33.1 vs. 19.4%; p < 0.01). Our findings demonstrate that a molar ratio of ascorbic acid and tea equal or superior to 0.25 or 0.50 is necessary to overcome the inhibitory effect in rats of tea prepared under Tunisian circumstances. In relation to human nutrition, for Tunisians who regularly drink tea, we suggest a much greater amount of ascorbic acid than that normally recommended for normal subjects.

Absorption↗

Effect of acute and chronic tea consumption on platelet aggregation in patients with coronary artery disease.

Epidemiological studies suggest that tea consumption is associated with a decreased risk of cardiovascular events, but the mechanisms of benefit remain undefined. Platelet aggregation is a precipitating event in cardiovascular disease, and tea contains antioxidant flavonoids that are known to decrease platelet aggregation in vitro. To test the effect of tea consumption on platelet aggregation, we randomized 49 patients with coronary artery disease to either 450 mL of black tea or water consumed initially, followed by 900 mL of tea or water daily for 4 weeks in a crossover design. Ex vivo platelet aggregation in platelet-rich plasma was assessed in response to ADP and thrombin receptor-activating peptide at baseline and 2 hours and 4 weeks after beverage consumption. We observed dose-dependent platelet aggregation in response to each agonist, and neither relation was altered by acute or chronic tea consumption. Plasma flavonoids increased with acute and chronic tea consumption, indicating adequate absorption of tea flavonoids. In conclusion, these results demonstrate that acute and chronic black tea consumption does not affect ex vivo platelet aggregation in patients with coronary artery disease. These findings suggest that an effect of tea flavonoids on platelet aggregation is unlikely to be the explanation for the reduction in risk of cardiovascular events noted in epidemiological studies.

Adenosine Diphosphate↗

Comparison of microdilution and disc diffusion methods in assessing the in vitro activity of fluconazole and Melaleuca alternifolia (tea tree) oil against vaginal Candida isolates.

The in vitro activity of fluconazole and Melaleuca alternifolia (tea tree) oil was evaluated against 99 vaginal Candida strains by the broth microdilution and disc diffusion methods. The microdilution method was performed in accordance with NCCLS-M27A guidelines. An investigational method was used for the disc diffusion test. Fluconazole and tea tree oil minimum inhibitory concentrations (MICs) obtained at 48 h tended to increase 1- to 2-fold or remain the same compared to 24 h readings for most of the isolates tested. C. krusei and C. norvegensis had significantly higher MICs and smaller inhibition zones for fluconazole compared to other species. Tea tree oil MICs were found to be similar, in general, for all Candida spp. tested. The geometric mean MIC of tea tree oil for all isolates was 2.2% (range, 0.25-4%) at 24 h and 3.0% (range, 1-8%) at 48 h. Tea tree oil mean inhibition zone diameter was 24 mm (range, 14-42 mm) at 24 h and 15.8 mm (range, 10-35 mm) at 48 h. In vitro activity of tea tree oil against fluconazole-resistant Candida strains was of particular interest. The isolates had similar tea tree oil MICs and inhibition zone diameters regardless of their fluconazole susceptibility profile. Tea tree oil MIC ranges (inhibition zone diameter ranges) were 2-4% (12-21 mm) and 2% (35 mm) at 48 h for C. krusei and C. norvegensis, respectively. These results suggest that tea tree oil MICs of the fluconazole-resistant isolates are comparable to those of fluconazole-susceptible isolates. This in vitro finding is promising for potential use of topical tea tree oil formulations in the treatment of candidiasis due to fluconazole-resistant strains.

Anti-Infective Agents, Local↗

Induction of apoptosis and cell cycle arrest in cancer cells by in vivo metabolites of teas.

The present study was conducted to determine in vivo possibilities of inducing apoptosis and cell cycle arrest in rat cancer cells by green, oolong, and black teas and also to further identify the mechanisms inhibiting cancer cell proliferation by the sera from tea-treated rats. The tea extracts from these three kinds of tea, the rat sera obtained after oral intubation of the tea extracts, and the tea polyphenolic compounds, (-)-epigallocatechin-3-gallate, (-)-epigallocatechin, (-)-epicatechin-3-gallate, and the aflavins, were used in the related tests. The extracts, the sera from the treated rats, and the polyphenolic compounds significantly inhibited the proliferation of a rat hepatoma cell line (AH109A) and murine B16 melanoma cells but not normal rat mesothelial (M) cells. (-)-Epicatechin exhibited synergistic effects with (-)-epigallocatechin-3-gallate, (-)-epicatechin-3-gallate, and theaflavins against AH109A cell proliferation. The fluorescence staining of the nuclei, electrophoresis detection of DNA fragmentation, and analysis of cell cycle indicated that the sera from the tea-treated rats, the tea extracts, and the related tea components resulted in loss of viability, apoptosis, and cell cycle arrest at the G1 phase in AH109A and/or B16 cells, but not in normal M cells. Our results suggest that induction of apoptosis and cell cycle arrest may be important mechanisms of in vivo proliferation inhibition of AH109A and other cancer cells by these teas.

Animals↗

Effects of green tea extract administration on the pharmacokinetics of clozapine in rats.

The pharmacokinetic interaction between clozapine, an atypical antipsychotic with metabolic complications, including weight gain, and green tea consumption has not been evaluated, although green tea is responsible for beneficial effects, including weight reduction, and is widely consumed in the world. Commercial green tea extract (175 mg kg(-1)) or saline was administered orally for 4 days before the oral administration of clozapine (20 mg kg(-1) ) to rats. Plasma concentrations of clozapine were measured up to 5 h after clozapine administration, and then hepatic CYP1A2 expression and activity were determined. There was no significant difference in the elimination half-life of clozapine between the green tea extract and saline groups. However, the time to reach peak concentration (T(max)) was significantly increased by green tea extract. The mean total area under the plasma concentration-time curve (AUC(0-infinity)) and maximal peak plasma concentration (C(max)) of clozapine in the green tea extract group were significantly lower than those of controls. Green tea extract induced a approximately 2-fold increase in hepatic CYP1A2 levels, while the activity increased slightly (by 10% of control). Because of this reduction in AUC and T(max) of clozapine by green tea extract pretreatment, we suggest that both the rate and amount of absorption of clozapine may be reduced by green tea extract, although the hepatic elimination phase may not be significantly altered. Therefore, the clinical implications of the effects of green tea on the bioavailability of clozapine in patients should be further evaluated.

Animals↗

Potential therapeutic properties of green tea polyphenols in Parkinson's disease.

Tea is one of the most frequently consumed beverages in the world. It is rich in polyphenols, a group of compounds that exhibit numerous biochemical activities. Green tea is not fermented and contains more catechins than black tea or oolong tea. Although clinical evidence is still limited, the circumstantial data from several recent studies suggest that green tea polyphenols may promote health and reduce disease occurrence, and possibly protect against Parkinson's disease and other neurodegenerative diseases. Green tea polyphenols have demonstrated neuroprotectant activity in cell cultures and animal models, such as the prevention of neurotoxin-induced cell injury. The biological properties of green tea polyphenols reported in the literature include antioxidant actions, free radical scavenging, iron-chelating properties, (3)H-dopamine and (3)H-methyl-4-phenylpyridine uptake inhibition, catechol-O-methyltransferase activity reduction, protein kinase C or extracellular signal-regulated kinases signal pathway activation, and cell survival/cell cycle gene modulation. All of these biological effects may benefit patients with Parkinson's disease. Despite numerous studies in recent years, the understanding of the biological activities and health benefits of green tea polyphenols is still very limited. Further in-depth studies are needed to investigate the safety and efficacy of green tea in humans and to determine the different mechanisms of green tea in neuroprotection.

Animals↗

Paradoxical effects of green tea (Camellia sinensis) and antioxidant vitamins in diabetic rats: improved retinopathy and renal mitochondrial defects but deterioration of collagen matrix glycoxidation and cross-linking.

We tested the hypothesis that green tea prevents diabetes-related tissue dysfunctions attributable to oxidation. Diabetic rats were treated daily with tap water, vitamins C and E, or fresh Japanese green tea extract. After 12 months, body weights were decreased, whereas glycated lysine in aorta, tendon, and plasma were increased by diabetes (P < 0.001) but unaffected by treatment. Erythrocyte glutathione and plasma hydroperoxides were improved by the vitamins (P < 0.05) and green tea (P < 0.001). Retinal superoxide production, acellular capillaries, and pericyte ghosts were increased by diabetes (P < 0.001) and improved by green tea and the vitamins (P variable). Lens crystallin fluorescence at 370/440 nm was ameliorated by green tea (P < 0.05) but not the vitamins. Marginal effects on nephropathy parameters were noted. However, suppressed renal mitochondrial NADH-linked ADP-dependent and dinitrophenol-dependent respiration and complex III activity were improved by green tea (P variable). Green tea also suppressed the methylglyoxal hydroimidazolone immunostaining of a 28-kDa mitochondrial protein. Surprising, glycoxidation in tendon, aorta, and plasma was either worsened or not significantly improved by the vitamins and green tea. Glucosepane cross-links were increased by diabetes (P < 0.001), and green tea worsened total cross-linking. In conclusion, green tea and antioxidant vitamins improved several diabetes-related cellular dysfunctions but worsened matrix glycoxidation in selected tissues, suggesting that antioxidant treatment tilts the balance from oxidative to carbonyl stress in the extracellular compartment.

Animals↗

Ingestion of green tea rapidly decreases prostaglandin E2 levels in rectal mucosa in humans.

The objective of this Phase I/II study was to assess the potential for green tea to be used as a colorectal cancer chemopreventive agent. This study measured the dose-related biological effects of administration of a single dose of green tea on the rectal mucosa of normal volunteers. Volunteers were admitted to the Robert Wood Johnson Medical School Clinical Research Center for 24 h. Baseline blood and rectal biopsy samples were obtained before the volunteers drank 0.6, 1.2, or 1.8 g of green tea solids dissolved in warm water. Blood samples were taken 2, 4, 8, and 24 h after the tea administration. Rectal biopsies were obtained at 4, 8, and 24 h. Prostaglandin E2 (PGE2) levels were analyzed by ELISA. Tea polyphenol levels in the blood, urine, and rectal tissue were measured by high-performance liquid chromatography using a Coulochem electrode array detection system. Statistical comparisons were made using ANOVA. Decreased levels of PGE2 in rectal mucosa were observed at 4 and 8 h after consumption of green tea. There was no correlation between inhibition of PGE2 and tissue or plasma levels of tea polyphenols. Ten of 14 subjects demonstrated a response to green tea, as evidenced by at least a 50% inhibition of PGE2 levels at 4 h. We conclude that green tea constituents have biological activity in inhibiting PGE2 synthesis. Given the 71% "response rate," we believe these data support the study of green tea as a colorectal chemopreventive agent in more long-term Phase II trials.

Administration, Oral↗

Comparative study of antioxidant potential of tea with and without additives.

Oxidative damage is one of the many mechanism leading to chronic diseases. Therefore interest is growing in the protection afforded by antioxidant nutrients against free radical reactions. More recently, the attention has shifted to polyphenols. Polyphenols are secondary plant metabolites occurring widely in plant food. They possess outstanding antioxidant properties, suggesting a possible protective role in man. Tea (Camellia sinensis) is a widely consumed beverage throughout the world containing polyphenols more than 35% of its dry weight. In the present work we have investigated the effect of tea without milk, tea with milk and lemon tea on the serum lipid peroxidation level (as a parameter of free radical generation). The results show that there were significant decrease in serum lipid peroxidation (Malonaldehyde) level half hour after ingestion of lemon tea and tea without milk which tends to normalize with increase in time. This decrease is much significant in case of lemon tea than tea without milk after half hour or one hour. Hence the interpretation is, tea without milk is a good source of antioxidant and addition of lemon to tea increases its antioxidant potential.

Adult↗

The effects on cell growth of tea polyphenols acting as a strong anti-peroxidatant and an inhibitor of apoptosis in primary cultured rat skin cells.

Studies during the past few years have indicated an inhibitory effect of green tea or tea polyphenols on tumorigenesis in animal and even in human. The purpose of this study was to observe the possible effects of tea polyphenols on skin cell growth and on apoptosis in rat primary cultured keratinocytes and fibroblasts. The release of a cell plasma enzyme (LDH), lipid peroxidation products (MDA production), and GSH-Px (glutathione peroxidase) into the medium in cultured cells was determined after treatment with tea polyphenols in a primary culture of skin cells. The percentage of cells in each cell cycle phase and in apoptosis were assayed by flow cytometry (FCM). Tea polyphenols may have a beneficial effect on skin cells at concentrations from 0.05% to 0.1%, showing a dose-dependent decrease in LDH, MDA (malondialdehyde) production, and a significant dose-dependent increase in GSH-Px and cell number. These effects were more obvious after exposure for 24 h than after 12 h. The results indicate that tea polyphenols may stabilize and protect the cell membrane against the release of cell plasma enzyme LDH, and its anti-peroxidation effect is also important for cell growth. FCM analysis revealed that treatment with 0.01% to 0.1% tea polyphenols decreased the percentage of cells in the G1/G0 (quiescent) phase from 81.32% to 74.38%, and increased the percentage of cells in S and G2/M phase from 9.87% to 15.26%, and from 6.51% to 10.36%, respectively. Tea polyphenols also increased the value of PI (proliferation index) from 18.17 to 25.62. At the same time it decreased the percentage of apoptosis from 27.10% to 17.97%, which indicates that green tea stimulates cell growth and inhibits the occurrence of apoptosis. Our results indicate that tea polyphenols are effective anti-oxidants and also inhibit apoptosis, which may improve the proliferative capacity of primary skin cells in vitro.

Animals↗

[Effect of a complex tea on reducing blood lipid in rabbits].

In order to observe the effect of a complex tea composed of tea, ginkgo leaf, red koji and fructus lycii on reducing blood lipids in experimental rabbits, 40 rabbits weighted from 1.5 to 2.0 kg were divided randomly into 5 group: (I) normal control group, (II) hyperlipidemia model(positive control), (III) green tea control group, (IV) low dose complex tea group, and (V) high dose complex tea group. Blood triglyceride(TG), cholesterol(TC), lower density lipoprotein(LDL) and high density lipoprotein(HDL) were measured before experiment and 6.12 weeks later. Then the pathological changes of heart, aorta and liver were observed. After 12 weeks of experiment, the results showed that, (1) hyperlipidemia characterized by high TC has been induced by high-fat feeds in group II, (2) the complex tea can reduce body weight and eliminate the lipids deposition in aorta and liver. (3) the complex tea can decrease serum TG, TC,LDL and increase serum HDL in the high complex tea group. The results indicate that the complex tea is more effective than green tea on reducing blood lipids in experimental rabbits.

Animals↗

Chemoprevention of oral cancer by green tea.

Green tea has been a popular beverage for many centuries. Only recently, however, has the anti-cancer power of green tea constituents been unveiled. Green tea polyphenols are found to induce apoptosis (programmed cell death) in many types of tumor cells, including oral cancer cells. However, mechanisms that enable normal cells to evade the apoptotic effect still are not understood. In this study, cell growth and invasion assays combined with apoptosis assays were used to examine the effects of green tea extracts, green tea polyphenols, and the most potent green tea polyphenol, (-)-epigallocatechin-3-gallate (EGCG), on normal human keratinocytes and oral carcinoma cells. The results showed that green tea and its constituents selectively induce apoptosis only in oral carcinoma cells, while EGCG was able to inhibit the growth and invasion of oral carcinoma cells. These differential responses to green tea and its constituents between normal and malignant cells were correlated with the induction of p57, a cell cycle regulator. These data suggest that the chemopreventive effects of green tea polyphenols may involve a p57 mediated survival pathway in normal epithelial cells, while oral carcinoma cells undergo an apoptotic pathway. Therefore, regular consumption of green tea could be beneficial in the prevention of oral cancer.

Antineoplastic Agents, Phytogenic↗

Effects of tea on preneoplastic lesions and cell cycle regulators in rat liver.

The effects of tea polyphenols and tea pigments on rat liver precancerous lesions and some cell cycle regulators were studied. A modified Solt-Farber model in rats was established by multiple low-dosage of N-nitrosodiethylamine (NDEA) i.p. injections, followed by i.p. CCl(4) injection and partial hepatectomy. Sixty male Wistar rats were randomly divided into four groups: positive control group, two tea-treated groups, and negative control group. Rats in tea-treated groups were given tea polyphenols (0.1%) and tea pigments (0.1%) in drinking fluid during the whole experiment. The number and area of glutathione S-transferase P (GST-P)-positive foci in the rat liver were used as biomarkers of precancerous liver lesions. Western blotting assay was carried out to detect the expression of cyclin D1, CDK4, and P21(WAF1/CIP1) on whole liver extract. At the end of the experiment (56 days), the number and area of GST-P-positive foci in liver increased significantly in carcinogen-administered positive control group, whereas no GST-P-positive foci were found in the negative control group in which animals did not receive carcinogen exposure. The number and area of GST-P-positive foci in tea-treated, carcinogen-exposed groups were significantly reduced as compared with the positive control group. It was also found that the expression of P21(WAF1/CIP1) was significantly induced and the expression of cyclin D1 and CDK4 was significantly inhibited in tea-treated groups. These results suggest that tea polyphenols and tea pigments are effective in preventing the precancerous liver lesions in rats, and modulation of cell cycle by regulating cell cycle regulators may be a possible mechanism.

Animals↗

[Chemopreventive effect of tea and curcumin on DMBA-induced oral carcinogenesis in hamsters].

0.5% DMBA solution (in mineral oil) was applied topically to the left cheek pouch of male Syrian golden hamsters 3 times per week for 6 weeks. After the last treatment of DMBA, the animals received 0.6% green tea powder as drinking fluid, or 10 mumol curcumin applied topically 3 times per week, or the combination of green tea and curcumin treatment, or no treatment for 18 weeks. The combination of tea and curcumin significantly decreased the oral visible tumor incidence and the squamous cell carcinoma (SCC) incidence. The combination of tea and curcumin also decreased the number of visible tumors and the tumor volume as well as the numbers of SCC, dysplasic lesions, and papillomas respectively. Green tea or curcumin treatment decreased the number of visible tumor, the tumor volume and the number of SCC respectively. Green tea also decreased the number of dysplasic lesions. Curcumin also significantly decreased the SCC incidence. Tea and curcumin, singly or in combination decreased bromodeoxyuridine (BrdU)-labeling index in hyperplasia, dysplasia, and papillomas. Tea alone and in combination with curcumin significantly increased the apoptotic index in dysplasia and SCC. Curcumin alone and in combination with tea inhibited the angiogenesis in papilloma and SCC. The results suggested that green tea and curcumin had inhibitory effects against oral carcinogenesis at the post-initiation stage and such inhibition may be related to the suppression of cell proliferation, induction of apoptosis, and inhibition of angiogenesis.

9,10-Dimethyl-1,2-benzanthracene↗