cancer-prevention

Author: Joshua D. Lambert and Ryan J. Elias

Green tea (Camellia sinensis) is rich in catechins, of which (−)-epigallocatechin-3-gallate (EGCG) is the most abundant. Studies in animal models of carcinogenesis have shown that green tea and EGCG can inhibit tumorigenesis during the initiation, promotion and progression stages. Many potential mechanisms have been proposed including both antioxidant and pro-oxidant effects, but questions remain regarding the relevance of these mechanisms to cancer prevention. In the present review, we will discuss the redox chemistry of the tea catechins and the current literature on the antioxidant and pro-oxidative effects of the green tea polyphenols as they relate to cancer prevention. We report that although the catechins are chemical antioxidants which can quench free radical species and chelate transition metals, there is evidence that some of the effects of these compounds may be related to induction of oxidative stress. Such pro-oxidant effects appear to be responsible for the induction of apoptosis in tumor cells. These pro-oxidant effects may also induce endogenous antioxidant systems in normal tissues that offer protection against carcinogenic insult. This review is meant point out understudied areas and stimulate research on the topic with the hope that insights into the mechanisms of cancer preventive activity of tea polyphenols will result.

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Author: Marco Assunção and Maria J. Santos-Marques and Félix Carvalho and José P. Andrade

Author: Martina Bancirova

Tea is a common beverage. The green tea is preferentially recommended for its strong antioxidant properties and also for its antimicrobial activity. The antioxidant capacities of 30 samples (black and green tea) were determined by the chemiluminescent Trolox equivalent antioxidant capacity (TEAC) determination. The average value of TEAC of the non-fermented (green tea) and semi-fermented tea samples was 1.43 mM and the average value of TEAC of the fermented teas (black tea) samples was 1.43 mM. All samples were stored in freezer (−20 °C) and the TEAC determination was repeated after a year. The average values of TEAC of non-fermented and semi-fermented tea samples were twofold lower in comparison to fermented tea samples and only 20% of average value of TEAC of the fresh tea infusion. The parallel determinations of minimal inhibitory concentration (MIC) on gram-positive and gram-negative bacterial strains (Enterococcus faecalis, Staphylococcus aureus, Pseudomonas aeruginosa and Escherichia coli) were done. Also the MIC was possible to determine after a year. The assumed prevailing antioxidant and antimicrobial activities of non-fermented tea infusions were not confirmed as well as the dominant antioxidant and antimicrobial properties of specific type of tea infusion.

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Author: Yan Xu and Jun-jian Zhang and Li Xiong and Lei Zhang and Dong Sun and Hui Liu

Responses to oxidative stress contribute to damage caused by chronic cerebral hypoperfusion, which is characteristic of certain neurodegenerative diseases. We used a rat model of chronic cerebral hypoperfusion to determine whether green tea polyphenols, which are potent antioxidants and free radical scavengers, can reduce vascular cognitive impairment and to investigate their underlying mechanisms of action. Different doses of green tea polyphenols were administered orally to model rats from 4 to 8 weeks after experimentally induced cerebral hypoperfusion, and spatial learning and memory were assessed using the Morris water maze. Following behavioral testing, oxygen free radical levels and antioxidative capability in the cortex and hippocampus were measured biochemically. The levels of lipid peroxidation and oxidative DNA damage were assessed by immunohistochemical staining for 4-hydroxynonenal and 8-hydroxy-2′-deoxyguanosine, respectively. Rats that received green tea polyphenols 400 mg/kg per day had better spatial learning and memory than saline-treated rats. Green tea polyphenols 400 mg/kg per day were found to scavenge oxygen free radicals, enhance antioxidant potential, decrease lipid peroxide production and reduce oxidative DNA damage. However, green tea polyphenols 100 mg/kg per day had no significant effects, particularly in the cortex. This study suggests that green tea polyphenols 400 mg/kg per day improve spatial cognitive abilities following chronic cerebral hypoperfusion and that these effects may be related to the antioxidant effects of these compounds.

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Author: Xiaobing Fan and Devkumar Mustafi and Marta Zamora and Jonathan N. River and Sean Foxley and Gregory S. Karczmar

The purpose of this research was to test whether dynamic contrast enhanced MRI could assess the effect of green tea on the angiogenic properties of transplanted rodent tumors. Copenhagen rats bearing AT6.1 prostate tumors inoculated in the hind limbs were randomly assigned to cages in which they were allowed to only drink either plain water (control group) or water containing green tea extract (treated group). Assignments were made after a baseline MRI experiment (week 0) was performed on each rat at 4.7 T. All the rats were subsequently imaged at day 7 (week 1) and day 14 (week 2) to follow tumor growth and vascular development. The two-compartment pharmacokinetic model was used to analyze the dynamic contrast Gd-DTPA enhanced MRI data on a pixel-by-pixel basis over the tumor area to obtain the volume transfer constant (Ktrans) and extravascular extracellular space (ve). An identity Chi-squared test showed that the distributions of averaged histograms (n=6) of Ktrans and ve were significantly different from week 0 to both weeks 1 and 2 (p<0.001) in both the control and the treated rats due to increasing areas of tumor necrosis. However, the tumor growth rate was statistically indistinguishable between control and treated rats. There was no significant difference in the distributions of Ktrans and ve between control and treated rats. The results showed that no effects of green tea on tumor micro-vasculature were measurable by dynamic Gd-DTPA enhanced MRI.

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Author: Lei Li and C.-Y. Oliver Chen and Giancarlo Aldini and Elizabeth J. Johnson and Helen Rasmussen and Yasukazu Yoshida and Etsuo Niki and Jeffrey B. Blumberg and Robert M. Russell and Kyung-Jin Yeum

Epigallocatechin gallate, a major component of green tea polyphenols, protects against the oxidation of fat-soluble antioxidants including lutein. The current study determined the effect of a relatively high but a dietary achievable dose of lutein or lutein plus green tea extract on antioxidant status. Healthy subjects (50–70 years) were randomly assigned to one of two groups (n=20 in each group): (1) a lutein (12 mg/day) supplemented group or (2) a lutein (12 mg/day) plus green tea extract (200 mg/day) supplemented group. After 2 weeks of run-in period consuming less than two servings of lightly colored fruits and vegetables in their diet, each group was treated for 112 days while on their customary regular diets. Plasma carotenoids including lutein, tocopherols, flavanols and ascorbic acid were analyzed by HPLC-UVD and HPLC-electrochemical detector systems; total antioxidant capacity by fluorometry; lipid peroxidation by malondialdehyde using a HPLC system with a fluorescent detector and by total hydroxyoctadecadienoic acids using a GC/MS. Plasma lutein, total carotenoids and ascorbic acid concentrations of subjects in either the lutein group or the lutein plus green tea extract group were significantly increased (P<.05) at 4 weeks and throughout the 16-week study period. However, no significant changes from baseline in any biomarker of overall antioxidant activity or lipid peroxidation of the subjects were seen in either group. Our results indicate that an increase of antioxidant concentrations within a range that could readily be achieved in a healthful diet does not affect in vivo antioxidant status in normal healthy subjects when sufficient amounts of antioxidants already exist.

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Author: Qi Dai and Xiao-Ou Shu and Honglan Li and Gong Yang and Martha J. Shrubsole and Hui Cai and Butian Ji and Wanqing Wen and Adrian Franke and Yu-Tang Gao and Wei Zheng

Background Studies have found that tea polyphenols inhibit aromatase. Because of the substantial difference in levels of estrogens between premenopausal and postmenopausal women, the relationship between tea consumption and breast cancer risk may depend on menopausal status. Methods We examined this hypothesis in the Shanghai Women's Health Study, a population-based cohort study of 74,942 Chinese women. Results We found a time-dependent interaction between green tea consumption and age of breast cancer onset (p for interaction, 0.03). In comparison with non-tea drinkers, women who started tea-drinking at 25 years of age or younger had a hazard ratio (HR) of 0.69 (95% confidence interval [CI]: 0.41–1.17) to develop premenopausal breast cancer. On the other hand, compared with non-tea drinkers, women who started tea drinking at 25 years of age or younger had an increased risk of postmenopausal breast cancer with an HR of 1.61 (95% CI: 1.18–2.20). Additional analyses suggest regularly drinking green tea may delay the onset of breast cancer. Conclusions Further studies are needed to confirm our findings.

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Author: Qiong Li and Haifeng Zhao and Ming Zhao and Zhaofeng Zhang and Yong Li

As the organism ages, production of reactive oxygen species (ROS) increases while antioxidants defense capability declines, leading to oxidative stress in critical cellular components, which further enhances ROS production. In the brain, this vicious cycle is more severe as brain is particularly vulnerable to oxidative damage. In our study, 14-month-old female C57BL/6J mice were orally administered 0.05% green tea catechins (GTC, w/v) in drinking water for 6 months. We found that GTC supplementation prevented the decrease in total superoxide dismutase and glutathione peroxidase activities in serum as well as reduced the thiobarbituric acid reactive substances and protein carbonyl contents in the hippocampus of aged mice. The activation of transcriptional factor nuclear factor-kappa B and lipofuscin formation in pyramidal cells of hippocampal CA1 region, which are all related to oxidative stress, was also reduced after GTC treatment. We also found that long-term GTC treatment prevented age-related reductions of two representative post-synaptic proteins post-synaptic density 95 and N-methyl-d-aspartate receptor 1 in the hippocampus. These results demonstrated that chronic 0.05% green tea catechins administration may prevent oxidative stress related brain aging in female C57BL/6J mice.

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Author: Shigeki Yanagi and Kazuaki Matsumura and Akira Marui and Manabu Morishima and Suong-Hyu Hyon and Tadashi Ikeda and Ryuzo Sakata

Objective Ischemia–reperfusion injury is among the most serious problems in cardiac surgery. Epigallocatechin-3-gallate, a major polyphenolic component of green tea, is thought to be cardioprotective through its antioxidant activities. We investigated cardioprotective effects of oral epigallocatechin-3-gallate pretreatment against ischemia–reperfusion injury in isolated rat hearts and considered possible underlying mechanisms. Methods Rats were given epigallocatechin-3-gallate solution orally at 0.1, 1, or 10 mmol/L (n = 12 per group) for 2 weeks; controls (n = 12) received tap water alone for 2 weeks. Subsequently, Langendorff-perfused hearts were subjected to global ischemia for 30 minutes, followed by 60 minutes of reperfusion. Results Recoveries at 60 minutes after reperfusion of left ventricular developed pressure and maximum positive and minimum negative first derivatives of left ventricular pressure were significantly higher in 1-mmol/L group than in 0.1-mmol/L (P < .0001), 10-mmol/L (P < .05), and control (P < .0001) groups. Oxidative stress after reperfusion, as reflected by 8-hydroxy-2′-deoxyguanosine index, was lower in 1-mmol/L group than in control (P < .01) and 0.1-mmol/L (P < .05) groups. Western blot analysis after reperfusion showed p38 activation and active caspase-3 expression to be lower in 1-mmol/L group than in control group (P < .05). Conclusions Oral pretreatment with epigallocatechin-3-gallate preserved cardiac function after ischemia–reperfusion, an effect that may involve its antioxidative, antiapoptotic properties, although a high dose did not lead to dramatic improvement in cardiac function. Oral epigallocatechin-3-gallate pretreatment may be a novel and simple cardioprotective method for preventing perioperative cardiac dysfunction in cardiac surgery.

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Author: Yoon Woo Koh and Eun Chang Choi and Sung Un Kang and Hye Sook Hwang and Mi Hye Lee and JungHee Pyun and RaeHee Park and YoungDon Lee and Chul-Ho Kim

Hepatocyte growth factor (HGF) and c-Met have recently attracted a great deal of attention as prognostic indicators of patient outcome, and they are important in the control of tumor growth and invasion. Epigallocatechin-3-gallate (EGCG) has been shown to modulate multiple signal pathways in a manner that controls the unwanted proliferation and invasion of cells, thereby imparting cancer chemopreventive and therapeutic effects. In this study, we investigated the effects of EGCG in inhibiting HGF-induced tumor growth and invasion of oral cancer in vitro and in vivo. We examined the effects of EGCG on HGF-induced cell proliferation, migration, invasion, induction of apoptosis and modulation of HGF/c-Met signaling pathway in the KB oral cancer cell line. We investigated the antitumor effect and inhibition of c-Met expression by EGCG in a syngeneic mouse model (C3H/HeJ mice, SCC VII/SF cell line). HGF promoted cell proliferation, migration, invasion and induction of MMP (matrix metalloproteinase)-2 and MMP-9 in KB cells. EGCG significantly inhibited HGF-induced phosphorylation of Met and cell growth, invasion and expression of MMP-2 and MMP-9. EGCG blocked HGF-induced phosphorylation of c-Met and that of the downstream kinases AKT and ERK, and inhibition of p-AKT and p-ERK by EGCG was associated with marked increases in the phosphorylation of p38, JNK, cleaved caspase-3 and poly-ADP-ribose polymerase. In C3H/HeJ syngeneic mice, as an in vivo model, tumor growth was suppressed and apoptosis was increased by EGCG. Our results suggest that EGCG may be a potential therapeutic agent to inhibit HGF-induced tumor growth and invasion in oral cancer.

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