Dual function of (−)-epigallocatechin gallate (EGCG) in healthy human lymphocytes

Kanadzu, Masaki; Lu, Yuquan; Morimoto, Kanehisa

doi:10.1016/j.canlet.2005.10.021

Cited by 61 publications

(51 citation statements)

References 19 publications

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“…This information reaffirmed that interactions with cell membrane for treatment with EGCG or Zn 2+ facilitated the decrease of membrane fluidity to result in anti-proliferation of LNCaP cells. Catechins or zinc ions are known to induce oxidative damage through the generation of reactive oxygen species Bishop et al, 2007;Kanadzu et al, 2006). Hence, it is likely that the generation of reactive oxygen species induced by catechins and zinc ions peroxidized membrane unsaturated fatty acids, which could lead to a decrease in membrane fluidity (Teresa et al, 2002 and structural characters of EGCG.…”

Section: +mentioning

confidence: 99%

Epigallocatechin-3-gallate affects the growth of LNCaP cells via membrane fluidity and distribution of cellular zinc

Yang

Sun

et al. 2009

J. Zhejiang Univ. Sci. B

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Abstract:Objective: To evaluate effects of epigallocatechin-3-gallate (EGCG) on the viability, membrane properties, and zinc distribution, with and without the presence of Zn . The proportion of EGCG incorporated into liposomes treated with the mixture of EGCG and Zn 2+ at the ratio of 1:1 was 90.57%, which was significantly higher than that treated with EGCG alone (30.33%). Electron spin resonance (ESR) studies and determination of fatty acids showed that the effects of EGCG on the membrane fluidity of LNCaP were decreased by Zn 2+. EGCG accelerated the accumulation of zinc in the mitochondria and cytosol as observed by atomic absorption spectrometer. Conclusion: These results show that EGCG interacted with cell membrane, decreased the membrane fluidity of LNCaP cells, and accelerated zinc accumulation in the mitochondria and cytosol, which could be the mechanism by which EGCG inhibits proliferation of LNCaP cells. In addition, high concentrations of Zn 2+ could attenuate the actions elicited by EGCG.

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Section: +mentioning

confidence: 99%

Epigallocatechin-3-gallate affects the growth of LNCaP cells via membrane fluidity and distribution of cellular zinc

Yang

Sun

et al. 2009

J. Zhejiang Univ. Sci. B

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“…Polyphenols can also induce a potentiation, rather than a reduction, of oxidative and radical chain processes, that is, they might act as "pro-oxidants". [31][32][33] Which behaviour predominates depends on the abundance of metal ions capable of maintaining a redox cycle and/or of redox-active enzymes, such as tyrosinases ("polyphenol oxidases") and peroxidases, on the ionchelating properties of the polyphenols themselves, and on pH. Additional factors could include the concentration of the polyphenol [33] and even the subcellular compartment involved.…”

Section: Introductionmentioning

confidence: 98%

A Mitochondriotropic Derivative of Quercetin: A Strategy to Increase the Effectiveness of Polyphenols

et al. 2008

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Mitochondria-targeted compounds are needed to act on a variety of processes that take place in these subcellular organelles and that have great pathophysiological relevance. In particular, redox-active molecules that are capable of homing in on mitochondria provide a tool to intervene on a major cellular source of reactive oxygen species and on the processes they induce, notably the mitochondrial permeability transition and cell death. We have linked the 3-OH of quercetin (3,3',4',5,7-pentahydroxy flavone), a model polyphenol, and the triphenylphosphonium moiety, a membrane-permeant cationic group, to produce proof-of-principle mitochondriotropic quercetin derivatives. The remaining hydroxyls were sometimes acetylated to hinder metabolism and improve solubility. The new compounds accumulate in mitochondria in a transmembrane potential-driven process and are only slowly metabolised by cultured human colon cells. They inhibit mitochondrial ATPase activity much as quercetin does, and are toxic for fast-growing cells.

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“…Similarly, Kanadzu et al (32) found that EGCG in concentrations ranging from 0.01 μmol L -1 to 10 μmol L -1 lowered DNA breakages in human lymphocytes, but also showed a strong genotoxic effect at higher concentrations (1 mmol L -1 ) (32).…”

Section: Comet Assaymentioning

confidence: 95%

Genotoxic Effects of Green Tea Extract on Human Laryngeal Carcinoma Cells In Vitro

Durgo

Kostić

Gradiški

et al. 2011

Archives of Industrial Hygiene and Toxicology

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Green tea (Camellia sinensis) contains several bioactive compounds which protect the cell and prevent tumour development. Phytochemicals in green tea extract (mostly fl avonoids) scavenge free radicals, but also induce pro-oxidative reactions in the cell. In this study, we evaluated the potential cytotoxic and prooxidative effects of green tea extract and its two main fl avonoid constituents epigallocatechin gallate (EGCG) and epicatechin gallate (ECG) on human laryngeal carcinoma cell line (HEp2) and its crossresistant cell line CK2. The aim was to see if the extract and its two fl avonoids could increase the sensitivity of the cisplatin-resistant cell line CK2 in comparison to the parental cell line. The results show that EGCG and green tea extract increased the DNA damage in the CK2 cell line during short exposure. The cytotoxicity of EGCG and ECG increased with the time of incubation. Green tea extract induced lipid peroxidation in the CK2 cell line. The pro-oxidant effect of green tea was determined at concentrations higher than those found in traditionally prepared green tea infusions.

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Dual function of (−)-epigallocatechin gallate (EGCG) in healthy human lymphocytes

Cited by 61 publications

References 19 publications

Epigallocatechin-3-gallate affects the growth of LNCaP cells via membrane fluidity and distribution of cellular zinc

Epigallocatechin-3-gallate affects the growth of LNCaP cells via membrane fluidity and distribution of cellular zinc

A Mitochondriotropic Derivative of Quercetin: A Strategy to Increase the Effectiveness of Polyphenols

Genotoxic Effects of Green Tea Extract on Human Laryngeal Carcinoma Cells In Vitro

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