Artifacts in Cell Culture: Rapid Generation of Hydrogen Peroxide on Addition of (−)-Epigallocatechin, (−)-Epigallocatechin Gallate, (+)-Catechin, and Quercetin to Commonly Used Cell Culture Media

Long, Lee Hua; Clément, Marie‐Véronique; Halliwell, Barry

doi:10.1006/bbrc.2000.2895

Cited by 361 publications

(262 citation statements)

References 40 publications

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“…We expanded upon this by further elucidating the precise mechanisms of CTN-triggered apoptosis in embryonic stem cells (Figures 3B-3E). Since previous papers have shown that the addition of some compounds to commonly-utilized cell culture media can trigger generation of ROS such as H 2 O 2 [39,40], I incubated CTN and culture medium together, and measured ROS by the ferrous iron oxidation-Xylenol Orange method [39]. The results showed no detectable artefactual ROS generation under these conditions (results not shown).…”

Section: Discussionmentioning

confidence: 92%

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

Chan

2007

Biochemical Journal

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The mycotoxin CTN (citrinin), a natural contaminant in foodstuffs and animal feeds, has cytotoxic and genotoxic effects on various mammalian cells. CTN is known to cause cell injury, including apoptosis, but the precise regulatory mechanisms of CTN action, particularly in stem cells and embryos, are currently unclear. In the present paper, I report that CTN has cytotoxic effects on mouse embryonic stem cells and blastocysts, and is associated with defects in their subsequent development, both in vitro and in vivo. Experiments in embryonic stem cells (ESC-B5) showed that CTN induces apoptosis via ROS (reactive oxygen species) generation, increased Bax/Bcl-2 ratio, loss of MMP (mitochondrial membrane potential), induction of cytochrome c release, and activation of caspase 3. In this model, CTN triggers cell death via inactivation of the HSP90 [a 90 kDa isoform of the HSP (heat-shock protein) family proteins]/multichaperone complex and subsequent degradation of Ras and Raf-1, further inhibiting anti-apoptotic processes, such as the Ras → ERK (extracellular-signal-regulated kinase) signal transduction pathway. In addition, CTN causes early developmental injury in mouse ESCs and blastocysts in vitro. Lastly, using an in vivo mouse model, I show that consumption of drinking water containing 10 µM CTN results in blastocyst apoptosis and early embryonic developmental injury. Collectively, these findings show for the first time that CTN induces ROS and mitochondria-dependent apoptotic processes, inhibits Ras → ERK survival signalling via inactivation of the HSP90/multichaperone complex, and causes developmental injury in vivo.

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Section: Discussionmentioning

confidence: 92%

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

Chan

2007

Biochemical Journal

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“…Recently, Long et al (2000) have demonstrated that the addition of GA, EGCG, EC, quercetin and catechin to commonly used cell culture media leads to generation of substantial amounts of hydrogen peroxide (H 2 O 2 ). The authors suggested that H 2 O 2 production by these phenolic compounds could be responsible of their effect on cells.…”

Section: Discussionmentioning

confidence: 99%

Flavonoids uptake and their effect on cell cycle of human colon adenocarcinoma cells (Caco2)

Salucci¹,

Stivala

Maiani³

et al. 2002

Br J Cancer

160

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Green tea, mainly through its constituents epigallocatechin gallate, epigallocatechin, epicatechin gallate and epicatechin, has demonstrated anticarcinogenic activity in several animal models, including those for skin, lung and gastro-intestinal tract cancer, although less is known about colorectal cancer. Quercetin, the major flavonoid present in vegetables and fruit, exerts potential anticarcinogenic effects in animal models and cell cultures, but less is known about quercetin glucosides. The objectives of this study were to investigate (i) the antioxidant activity of the phenolic compounds epicatechin, epigallocatechin gallate, gallic acid and quercetin-3-glucoside; (ii) the cytotoxicity of different concentrations of epicatechin, epigallocatechin gallate, and gallic acid; (iii) the cellular uptake of epicatechin, epigallocatechin gallate, gallic acid and quercetin-3-glucoside and (iv) their effect on the cell cycle. Human colon adenocarcinoma cells were used as experimental model. The results of this study indicate that all dietary flavonoids studied (epicatechin, epigallocatechin gallate, gallic acid and quercetin-3-glucoside) show a significant antioxidant effect in a chemical model system, but only epigallocatechin gallate or gallic acid are able to interfere with the cell cycle in Caco2 cell lines. These data suggest that the antioxidant activity of flavonoids is not related to the inhibition of cellular growth. From a structural point of view, the galloyl moiety appears to be required for both the antioxidant and the antiproliferative effects. Epidemiological studies from around the world have consistently reported that a high intake of fruit and vegetables is associated with a low incidence of most types of cancer (Wang et al, 1989;Dragsted et al, 1993). It is estimated that about 70% of all cancers are attributable to the diet. Colorectal cancer is the second most prevalent cancer in the developed world (Parkin et al, 1985). Western diet with a high intake of calories from fat and low fibre supply has been linked to an increase of colon cancer incidence, whilst vegetarian or mediterranean diets are more protective (Vargas and Alberts, 1992). Several compounds have been identified in plants which have well recognised antioxidant properties, such as carotenoids, ascorbic acid, a-tocopherol and flavonoids (Block et al, 1992;Hertog et al, 1992) and inhibit cancer development.Thus, the use of natural substances, that are derived from the diet for chemoprevention, might provide a strategy to inhibit the development of cancer. Green tea, mainly through its constituents epigallocatechin gallate (EGCG), epigallocatechin (EGC), epicatechin gallate (ECG) and epicatechin (EC), has demonstrated anticarcinogenic activity in several animal models, including those for skin, lung and gastro-intestinal tract cancer (Katiyar et al, 1992;Yang and Wang, 1993). Several recent studies (Berger et al, 2001;Uesato et al, 2001) on the effect of green tea polyphenolics on colon cancer cell lines have shown antiproliferative acti...

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“…In fact, most free-radical scavengers act on reversible oxidation -reduction reactions, and some phenolic phytochemicals can act both as antioxidants and prooxidants depending on their structure and the conditions. The metal-mediated autooxidation of some polyphenols generates semiquinone radicals, resulting in the enhancement of redox activity that produces ROS including hydrogen peroxide [50,69]. The prooxidant activity is thought to be directly proportional to the total number of hydroxyl groups.…”

Section: Possible Prooxidant Activity and Carcinogenicity Of Some Polmentioning

confidence: 99%

“…In addition, copper (which is present in the mammalian cell nucleus) is believed to play a central role in the formation of ROS, and result in DNA damage leading to neuronal toxicity and cell death. Thus, the metal-mediated autooxidation of some polyphenols generates semiquinone radicals, resulting in the enhancement of redox activity to produce ROS including hydrogen peroxide, which may contribute to the development of cancer [50,69]. The possible prooxidant activities and carcenogenicities of the aforementioned is shown schematically in Fig.…”

Section: Possible Prooxidant Activity and Carcinogenicity Of Some Polmentioning

confidence: 99%

The roles of polyphenols in cancer chemoprevention

2006

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Abstract.Oxidative stress imposed by reactive oxygen species (ROS) plays a crucial role in the pathophysiology associated with neoplasia, atherosclerosis, and neurodegenerative diseases. The ROS-induced development of cancer involves malignant transformation due to altered gene expression through epigenetic mechanisms as well as DNA mutations. Considerable attention has been focused on identifying naturally occurring antioxidative phenolic phytochemicals that are able to decrease ROS levels, but the efficacies of antioxidant therapies have been equivocal at best. Several studies have shown that some antioxidants exhibit prooxidant activity under certain conditions and potential carcinogenicity under others, and that dietary supplementation with large amounts of a single antioxidant may be deleterious to human health. This article reviews the intracellular signaling pathways that respond to oxidative stress and how they are modulated by naturally occurring polyphenols. The possible toxicity and carcinogenicity of polyphenols is also discussed.

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Artifacts in Cell Culture: Rapid Generation of Hydrogen Peroxide on Addition of (−)-Epigallocatechin, (−)-Epigallocatechin Gallate, (+)-Catechin, and Quercetin to Commonly Used Cell Culture Media

Cited by 361 publications

References 40 publications

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

Flavonoids uptake and their effect on cell cycle of human colon adenocarcinoma cells (Caco2)

The roles of polyphenols in cancer chemoprevention

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