Green tea supplementation increases glutathione and plasma antioxidant capacity in adults with the metabolic syndrome

Green tea, a popular polyphenol-containing beverage, has been shown to alleviate clinical features of the metabolic syndrome. However, its effects in endogenous antioxidant biomarkers are not clearly understood. Thus, we tested the hypothesis that green tea supplementation will upregulate antioxidant parameters (enzymatic and nonenzymatic) in adults with the metabolic syndrome. Thirty-five obese participants with the metabolic syndrome were randomly assigned to receive one of the following for 8 weeks: green tea (4 cups per day), control (4 cups water per day), or green tea extract (2 capsules and 4 cups water per day). Blood samples and dietary information were collected at baseline (0 week) and 8 weeks of the study. Circulating carotenoids (α-carotene, β-carotene, lycopene) and tocopherols (α-tocopherol, γ-tocopherol) and trace elements were measured using high-performance liquid chromatography and inductively coupled plasma mass spectroscopy, respectively. Serum antioxidant enzymes (glutathione peroxidase, glutathione, catalase) and plasma antioxidant capacity were measured spectrophotometrically. Green tea beverage and green tea extract significantly increased plasma antioxidant capacity (1.5 to 2.3 μmol/L and 1.2 to 2.5 μmol/L, respectively; P < .05) and whole blood glutathione (1783 to 2395 μg/g hemoglobin and 1905 to 2751 μg/g hemoglobin, respectively; P < .05) vs controls at 8 weeks. No effects were noted in serum levels of carotenoids and tocopherols and glutathione peroxidase and catalase activities. Green tea extract significantly reduced plasma iron vs baseline (128 to 92μg/dL, P < .02), whereas copper, zinc, and selenium were not affected. These results support the hypothesis that green tea may provide antioxidant protection in the metabolic syndrome.     

Protective effects of epigallocatechin gallate after UV irradiation of cultured human lens epithelial cells

PURPOSE: To evaluate the protective effects of epigallocatechin gallate (EGCG) against UV irradiation of cultured human lens epithelial cells. METHODS: We irradiated cultured human lens epithelial cells with a 30-second pulse from a UV lamp with an irradiance of 0.6 mW/cm(2). Five minutes and 1 hour after UV irradiation, we administered 0, 5, 10, 15, 25, 50, or 100 uM EGCG. The cell number was measured with a microscopic counting chamber and cell viability was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. RESULTS: Compared to untreated cells, the total number of cultured human lens epithelial cells was markedly higher after UV irradiation. In a dose-dependent manner, viability was also higher in EGCG-treated cells. CONCLUSIONS: EGCG increased the cell count and cell viability after UV irradiation of cultured human lens epithelial cells, indicating that EGCG can protect lens epithelium against UV damage.     

表没食子儿茶素没食子酸酯逆转多药耐药肝癌细胞株基因表达谱变化

目的:采用基因芯片技术获取表没食子儿茶素没食子酸酯(epigallocatechin gallate,EGCG)逆转肝癌多药耐药(multi-drug resistance,MDR)细胞前后的基因表达谱变化,探讨EGCG的可能耐药逆转作用机制。方法:cDNA微阵列分析EGCG作用肝癌MDR细胞株BEL7404/ADM前后的基因表达谱差异,Western Blot法检测细胞Cyclin G1蛋白表达变化以验证基因芯片分析的结果。结果:相对BEL7404/ADM细胞组,EGCG作用后细胞双荧光通路显著差异基因210个,上调表达38个,下调表达172个。与EGCG可能逆转耐药相关的基因有ABCB10(MDR/TAP),TOP2A,TOP2B,CCNG1上调,ABCB1,MVP,ARHD,HDAC5,GSS,GSTPI,HSPA1B,HSPB7,CDKN1A,RAB11B,RAB9P40下调等。Cyclin G1蛋白表达增加,符合cDNA微阵列基因水平变化。结论:EGCG多基因、多环节、多途径改变参与逆转ADM诱导的肝癌MDR,Western blot与基因芯片分析结果一致。     

Epigallocatechin gallate sensitizes cisplatin‐resistant oral cancer CAR cell apoptosis and autophagy through stimulating AKT/STAT3 pathway and suppressing multidrug resistance 1 signaling

Epigallocatechin gallate (EGCG) is a green tea polyphenol that presents anticancer activities in multiple cancer cells, but no available report was addressed for the underling molecular mechanism of cytotoxic impacts on drug‐resistant oral squamous cell carcinoma cells. In the present study, the inhibitory effects of EGCG were experienced on cisplatin‐resistant oral cancer CAR cells. EGCG inhibited cell viability in a time‐ and concentration‐dependent manner by a sulforhodamine B (SRB) assay. EGCG induced CAR cell apoptosis and autophagy by 4′,6‐diamidino‐2‐phenylindole (DAPI) dye, acridine orange (AO) staining and green fluorescent protein (GFP)‐tagged LC3B assay, respectively. EGCG also significantly enhanced caspase‐9 and caspase‐3 activities by caspase activity assay. EGCG markedly increased the protein levels of Bax, cleaved caspase‐9, cleaved caspase‐3, Atg5, Atg7, Atg12, Beclin‐1, and LC3B‐II, as well as significantly decreased the expression of Bcl‐2, phosphorylated AKT (Ser473) and phosphorylation of STAT3 on Tyr705 by western blotting in CAR cells. Importantly, the protein and gene expression of multidrug resistance 1 (MDR1) were dose‐dependently inhibited by EGCG. Overall, downregulation of MDR1 levels and alterations of AKT/STAT3 signaling contributed to EGCG‐induced apoptosis and autophagy in CAR cells. Based on these results, EGCG has the potential for therapeutic effect on oral cancer and may be useful for long‐term oral cancer prevention in the future. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 845–855, 2017.     

茶多酚诱导膀胱癌EJ细胞株凋亡与细胞内钙离子变化的相关性

目的：探讨茶多酚对膀胱癌EJ细胞株抑制增殖的分子机理。方法：采用流式细胞术、噻唑蓝(MTT)比色法和激光共聚焦成像技术，分别测定膀胱癌EJ细胞株的凋亡状态、细胞的周期变化、线粒体功能及细胞内离子钙浓度水平变化。用茶多酚处理EJ肿瘤细胞。结果：细胞的周期依浓度的改变而变化，浓度增加至20μg／ml发生明显的凋亡，OD值与浓度呈负相关性。细胞内钙离子浓度与时间、浓度的增加呈量效正相关。钙离子浓度逐渐升高亦呈现为时效、量效正相关性。结论：茶多酚能影响肿瘤细胞的增殖、凋亡过程。茶多酚诱导所致线粒体变化、细胞内钙离子超载可能在肿瘤凋亡中起着重要作用。     

Anticarcinogenic Activity of Green Tea Polyphenols

The main physiologically active polyphenol in green tea extractis (–)-epigallocatechin gallate (EGCG). Green tea extracthas an advantage over EGCG as a cancer chemopreventive agentfor humans, as is apparent from the Japanese custom of injestinggreen tea on a daily basis. Green tea extract similarly inhibitedprotein kinase C activation by teleocidin, a tumor promoter,as did EGCG. In addition, EGCG and green tea extract showedinhibitory effects on the growth of lung and mammary cancercell lines with similar potencies. An experiment using the estrogen-dependentMCF-7 cell line showed the mechanisms of action of these compoundsto be inhibiting the interaction of estrogen with its receptors.Considering our previous results of a single application ofEGCG to mouse skin inhibiting the specific binding of ³H-12-0-tetradecanoylphorbol-13-acetate(³H-TPA) and ³H-okadaic acid, we postulated that EGCG and compoundsin green tea extracts would block the interaction of tumor promoters,hormones and growth factors with their receptors: a kind ofsealing effect. The sealing effect would account for reversiblegrowth arrest, and may be induced by various kinds of compond.     

Effects Of Dietary Fat, Butylated Hydroxytoluene And Propyl Gallate On Microsomal Drug Metabolism In Rats

Dietary butylated hydroxytoluene, but not propyl gallate, increased liver size, microsomal cytochrome P₄₅₀ concentration and related drug metabolism. The kind and amount of dietary fat did not alter the effects of either antioxidant.     

The sensitizing capacity of the antioxidants propyl, octyl, and dodecyl gallate and some related gallic acid esters

8 alkyl gallates, including the widely used antioxidants propyl, octyl, and dodecyl (= lauryl) gallate, have been subjected to experimental sensitization in guinea pigs. Using a modern sensitization procedure, the results showed that all gallates are moderate to strong contact sensitizers: dodecyl (= lauryl) gallate was found to be the strongest. A characteristic correlation between side chain length and mean response was observed, giving a maximum of sensitization at a length of 12 carbon atoms (dodecyl gallate). A literature review revealed that the frequency of reports of allergic contact dermatitis from antioxidants of the gallate type has increased in the last 4 years. In most cases, the moderate sensitizer propyl gallate was the source of sensitization.     

Mutachromosomal effects of tert-butylhydroquinone in bone-marrow cells of mice

When given to mice either in a single ip injection of 200 mg/kg body weight or in 30 daily oral doses of 2 mg/kg, tert-butylhydroquinone had severe clastogenic effects on the bone-marrow cells. However mitostatic activity was observed only with the acute treatment.