The effect of epigallocatechin gallate on hepatocytes isolated from normal and partially hepatectomized rats

Mezera, Vojtěch; Kučera, Otto; Moravcová, Alena; Peterová, E; Červinková, Z

doi:10.1139/cjpp-2014-0069

Cited by 5 publications

(6 citation statements)

References 15 publications

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“…Our observations of proapoptotic action of EGCG are in accord with our previous study [ 59 ] as well as with findings of other authors [ 11 , 52 , 67 ] but at variance with some others [ 49 ]. In our experiment, EGCG-induced apoptosis was proved by caspase 3 activity, DAPI staining, and oligonucleosomal DNA fragmentation (data not shown).…”

Section: Discussionsupporting

confidence: 94%

“…It was suggested that green tea extract may be less toxic due to the presence of other compounds, such as vitamin C [ 46 ]. On the other hand, the toxic concentration found in the present study is the same as in our previous study in hepatocytes isolated from rats after partial hepatectomy or laparotomy [ 59 ].…”

Section: Discussionsupporting

confidence: 89%

“…Susceptibility to extrinsic apoptotic pathway was analyzed by El Naga et al, who reported upregulation of TRAIL death receptors in HepG2 cells after treatment with 153 μ mol/L EGCG [ 67 ]. However, we were not able to reproduce their findings in our previous study [ 59 ]. It is possible that the EGCG-induced death receptor upregulation is specific for cancer cell lines or occurs after very high concentrations of EGCG.…”

Section: Discussioncontrasting

confidence: 63%

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In VitroToxicity of Epigallocatechin Gallate in Rat Liver Mitochondria and Hepatocytes

Kučera

Mezera

Moravcová

et al. 2015

Oxidative Medicine and Cellular Longevity

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Epigallocatechin-3-gallate (EGCG) is the main compound of green tea with well-described antioxidant, anti-inflammatory, and tumor-suppressing properties. However, EGCG at high doses was reported to cause liver injury. In this study, we evaluated the effect of EGCG on primary culture of rat hepatocytes and on rat liver mitochondria in permeabilized hepatocytes. The 24-hour incubation with EGCG in concentrations of 10 μmol/L and higher led to signs of cellular injury and to a decrease in hepatocyte functions. The effect of EGCG on the formation of reactive oxygen species (ROS) was biphasic. While low doses of EGCG decreased ROS production, the highest tested dose induced a significant increase in ROS formation. Furthermore, we observed a decline in mitochondrial membrane potential in cells exposed to EGCG when compared to control cells. In permeabilized hepatocytes, EGCG caused damage of the outer mitochondrial membrane and an uncoupling of oxidative phosphorylation. EGCG in concentrations lower than 10 μmol/L was recognized as safe for hepatocytes in vitro.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 89%

Section: Discussioncontrasting

confidence: 63%

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In VitroToxicity of Epigallocatechin Gallate in Rat Liver Mitochondria and Hepatocytes

Kučera

Mezera

Moravcová

et al. 2015

Oxidative Medicine and Cellular Longevity

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“…In contrast, high doses of EGCG were found to be hepatotoxic [8, 11–13]. Similarly, EGCG displayed toxicity on mitochondria in permeabilized hepatocytes [8] and on mitochondria in a hepatoma cell line [14].…”

Section: Introductionmentioning

confidence: 99%

Effects of Epigallocatechin Gallate on Tert‐Butyl Hydroperoxide‐Induced Mitochondrial Dysfunction in Rat Liver Mitochondria and Hepatocytes

Mezera

Endlicher

Kučera

et al. 2016

Oxidative Medicine and Cellular Longevity

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Epigallocatechin gallate (EGCG) is a green tea antioxidant with adverse effects on rat liver mitochondria and hepatocytes at high doses. Here, we assessed whether low doses of EGCG would protect these systems from damage induced by tert-butyl hydroperoxide (tBHP). Rat liver mitochondria or permeabilized rat hepatocytes were pretreated with EGCG and then exposed to tBHP. Oxygen consumption, mitochondrial membrane potential (MMP), and mitochondrial retention capacity for calcium were measured. First, 50 μM EGCG or 0.25 mM tBHP alone increased State 4 Complex I-driven respiration, thus demonstrating uncoupling effects; tBHP also inhibited State 3 ADP-stimulated respiration. Then, the coexposure to 0.25 mM tBHP and 50 μM EGCG induced a trend of further decline in the respiratory control ratio beyond that observed upon tBHP exposure alone. EGCG had no effect on MMP and no effect, in concentrations up to 50 μM, on mitochondrial calcium retention capacity. tBHP led to a decline in both MMP and mitochondrial retention capacity for calcium; these effects were not changed by pretreatment with EGCG. In addition, EGCG dose-dependently enhanced hydrogen peroxide formation in a cell- and mitochondria-free medium. Conclusion. Moderate nontoxic doses of EGCG were not able to protect rat liver mitochondria and hepatocytes from tBHP-induced mitochondrial dysfunction.

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“…Undoubtedly, there are numerous benefits in using EGCG in the diet of a healthy individual and biochemically, and, specifically, cytologically effects have been studied in detail. Cytoprotective effects ascribed to this compound have been identified in the liver, kidney, heart, and lungs (Mezera et al, 2014;Kucera et al, 2015). Nuclear factor erythroid 2 -related factor 2 (NRF2) is a key regulator of the cellular antioxidant response.…”

Section: Green Tea Polyphenols (Gtps)mentioning

confidence: 99%

Epigallocatechin-3-Gallate Toxicity in Children: A Potential and Current Toxicological Event in the Differential Diagnosis With Virus-Triggered Fulminant Hepatic Failure

Sergi

2020

Front. Pharmacol.

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The use of nutraceuticals is considerably increasing worldwide with a demand for organic and clean foods in the last two decades, which is probably incomparable with other periods of our civilization. The consistent application of nutraceuticals and so-called "superfood" may have remarkable effects on the prevention of several chronic diseases, including cancer. Moreover, the increased rate of overweight and obesity in Western countries does not spare childhood and youth, and the number of parents using natural remedies for preventing pediatric illness is vastly increasing worldwide. However, the overwhelming effects on diseases often overshadow the side effects of such nutrition, particularly in societies without millennial experience with botanicals and natural elements. Thus, the final result may be disastrous for some individuals. The liver is the most important and conspicuous target organ of numerous molecular compounds, and the cell damage is particularly striking on the infantile and pediatric liver due to the immaturity of the hepatocytes. Here, we target some generic data on fulminant hepatic failure, the benefits, and toxicity of epigallocatechin-3-gallate, which is one of the major components of green tea, and the histopathology of the "green-tea"-associated liver disease.

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The effect of epigallocatechin gallate on hepatocytes isolated from normal and partially hepatectomized rats

Cited by 5 publications

References 15 publications

In VitroToxicity of Epigallocatechin Gallate in Rat Liver Mitochondria and Hepatocytes

In VitroToxicity of Epigallocatechin Gallate in Rat Liver Mitochondria and Hepatocytes

Effects of Epigallocatechin Gallate on Tert‐Butyl Hydroperoxide‐Induced Mitochondrial Dysfunction in Rat Liver Mitochondria and Hepatocytes

Epigallocatechin-3-Gallate Toxicity in Children: A Potential and Current Toxicological Event in the Differential Diagnosis With Virus-Triggered Fulminant Hepatic Failure

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