Safety studies on epigallocatechin gallate (EGCG) preparations. Part 1: Genotoxicity

Isbrucker, Richard; Bausch, Jochen; Edwards, John S.; Wolz, E.

doi:10.1016/j.fct.2005.07.005

Cited by 137 publications

(104 citation statements)

References 30 publications

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“…A significant increase in the level of MDA-DNA adducts was observed in 4-NQO induced animals, this may be due to the production of MDA a highly reactive aldehyde which forms adduct with DNA. Treatment with GTP to 4-NQO induced animals depicted a significant decrease in the level of MDA-DNA adducts, this might be due to inhibition of oxidative stress by GTP, thereby reducing the production of MDA and ultimately DNA adducts which correlated with the previous studies by Isbrucker et al, (2006).…”

Section: Discussionsupporting

confidence: 78%

Green Tea Polyphenol Protection Against 4-Nitroquinoline 1-Oxide-Induced Bone Marrow Lipid Peroxidation and Genotoxicity in Wistar Rats

Pandurangan

Periasamy²,

Anandasadagopan³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Asian Pacific J Cancer Prev, 13,[4107][4108][4109][4110][4111][4112] Introduction 4-NQO is a water soluble oral carcinogen which produces papilloma and invasive squamous cell carcinoma, resulting in clinical and histologic changes which is similar to those observed in neoplasms of humans (Fisker, 1990). 4-NQO is known to induce multi-step carcinogenesis. 4-NQO is also known to induce H-ras mutation in chromosome 7 leading to head and neck squamous cell carcinoma in experimental murine model, which is quite similar to that of tumours that develop in tobacco chewers (Hendler et al., 1996;Srinivasan et al., 2004;Srinivasan et al., 2006;Srinivasan et al., 2007).In experimental animals, the oral mucosa is relatively resistant to the carcinogenic effects of test compounds (Ito, 1981). However, application of 4-nitroquinoline-N-oxide (NQO) directly to the rat tongue (painting) or in the drinking water (Tanaka et al., 1993) induces squamous cell carcinoma. The potent activity of NQO provides a useful model for oral carcinogenesis (Eveson, 1981). Subcutaneous administration of NQO yielded lung adenoma, uterine leiomyosarcoma, soft tissue sarcoma and fibro sarcoma, etc., administration of NQO by stomach tube, yielded adenocarcinoma, papilloma and

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Section: Discussionsupporting

confidence: 78%

Green Tea Polyphenol Protection Against 4-Nitroquinoline 1-Oxide-Induced Bone Marrow Lipid Peroxidation and Genotoxicity in Wistar Rats

Pandurangan

Periasamy²,

Anandasadagopan³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Toxicity in mice often was observed in the form of increased alanine-aminotransferase levels suggesting hepatotoxicity [192], and/ or by oxidative stress [191]. Plasma EGCG concentrations in mice tend to be closer to levels reported in human studies compared to levels in rats, in which administration of similar doses results in higher plasma concentrations [188]. Chronic toxicity studies in beagle dogs, showed 67% lethality within 26 weeks of daily doses of 200-800 mg/kg Polyphenon E, a pure and standardized green tea extract, when the dogs fasted for 20 h prior to EGCG administration [193].…”

Section: Effects On Ttr Toxicity In Vivomentioning

confidence: 91%

“…Cell assays in bacteria and mouse lymphoma L5178Y tk +/-have shown that up to 450 μM EGCG were not genotoxic [188]. In animal experiments, a daily dose of up to ~1,000 mg/kg EGCG did not show teratogenicity in rats [189].…”

Section: Effects On Ttr Toxicity In Vivomentioning

confidence: 91%

Modulators of amyloid protein aggregation and toxicity: EGCG and CLR01

Attar

Rahimi

Bitan

2013

Translational Neuroscience

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Abnormal protein folding and self-assembly causes over 30 cureless human diseases for which no diseasemodifying therapies are available. The common side to all these diseases is formation of aberrant toxic protein oligomers and amyloid fibrils. Both types of assemblies are drug targets, yet each presents major challenges to drug design, discovery, and development. In this review, we focus on two small molecules that inhibit formation of toxic amyloid protein assemblies -the green-tea derivative (-)-epigallocatechin-3-gallate (EGCG), which was identified through a combination of epidemiologic data and a compound library screen, and the molecular tweezer CLR01, whose inhibitory activity was discovered in our group based on rational reasoning, and subsequently confirmed experimentally. Both compounds act in a manner that is not specific to one particular protein and thus are useful against a multitude of amyloidogenic proteins, yet they act via distinct putative mechanisms. CLR01 disrupts protein aggregation through specific binding to lysine residues, whereas the mechanisms underlying the activity of EGCG are only recently beginning to unveil. We discuss current in vitro and, where available, in vivo literature related to EGCG and CLR01's effects on amyloid β-protein, α-synuclein, transthyretin, islet amyloid polypeptide, and calcitonin. We also describe the toxicity, pharmacokinetics, and mechanism of action of each compound.

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“…Isbrucker et al [138] have also found no genotoxic concern with a epigallocatechin gallate (GTE) preparation, Teavigo. On the other hand, many studies have demonstrated that tea catechins could suppress the genotoxic activity of various carcinogens with both in vitro and in vivo systems.…”

Section: Effects Of Tea On Mutation and Genotoxictymentioning

confidence: 99%