Mitochondrial and Nuclear DNA Damage Induced by Curcumin in Human Hepatoma G2 Cells

Cao, Jun; Li, Jia; Zhou, Huimin; Liu, Yong; Zhong, Laifu

doi:10.1093/toxsci/kfj153

Cited by 203 publications

(129 citation statements)

References 33 publications

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“…The induction of DNA damage that we observed in HEp-2 and 7T cells following the treatment with curcumin is in agreement with those previously reported, despite differences in the type of cells and experimental conditions used (Cao et al, 2006;Huang et al, 2011;Jiang et al, 2010;Lin et al, 2008;Lopez-Lazaro et al, 2007;Su et al, 2006;Urbina-Cano et al, 2006). Although we have expected that more oxidative DNA damage (like oxidized purines) would appear in HEp-2 and 7T cells because of ROS induction, strand breaks were predominant and correlated with cytotoxicity.…”

Section: Discussionsupporting

confidence: 93%

Carboplatin resistant human laryngeal carcinoma cells are cross resistant to curcumin due to reduced curcumin accumulation

Rak

Čimbora‐Zovko

Gajski

et al. 2013

Toxicology in Vitro

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Section: Discussionsupporting

confidence: 93%

Carboplatin resistant human laryngeal carcinoma cells are cross resistant to curcumin due to reduced curcumin accumulation

Rak

Čimbora‐Zovko

Gajski

et al. 2013

Toxicology in Vitro

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“…[22][23][24][25][26][27][28][29][30] For instance, curcumin concentrations of 2.5 and 5 lg mL À1 were shown to induce DNA damage to both the mitochondrial and nuclear genomes in cells. 28 These reports raise concern about curcumin safety, as the induction of DNA alterations is a common event in carcinogenesis.…”

Section: Dear Editormentioning

confidence: 99%

“…40,[44][45][46][47][48] Experimental studies have demonstrated that, although low concentrations of curcumin induce antioxidant effects, higher concentrations of this compound increase the cellular levels of ROS. 4,9,23,28,[49][50][51][52][53] The presence of 2 a,b-unsaturated ketones in the chemical structure of curcumin may also mediate some of its negative properties. These chemical groups are known to react covalently with exposed thiol groups of cysteine residues of proteins through a reaction termed Michael addition.…”

Section: Dear Editormentioning

confidence: 99%

The dark side of curcumin

Burgos-Morón

Calderón-Montaño

Salvador

et al. 2010

Intl Journal of Cancer

303

210

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Dear Editor,Curcumin is a yellow-orange pigment obtained from the plant Curcuma longa. The powdered rhizome of this plant, called turmeric, is a common ingredient in curry powders and has a long history of use in traditional Asian medicine for a wide variety of disorders. In the last decade a large number of reports have been published on the beneficial effects of curcumin, and it has repeatedly been claimed that this natural product is efficient and safe for the prevention and treatment of several diseases including cancer. 1-3 It is not surprising, therefore, that curcumin is currently sold as a dietary supplement and that numerous clinical trials are ongoing or recruiting participants to evaluate curcumin activity. But there is accumulating evidence that curcumin may not be so effective and safe. Because such evidence is not generally acknowledged, the purpose of this letter is to briefly review the negative properties of curcumin so that they can be balanced against its beneficial effects.Most of the evidence that supports the therapeutic potential of curcumin is mainly based on in vitro studies in which curcumin was tested at concentrations in the micromolar range. Several reports have demonstrated, however, that the plasma concentrations of curcumin in people taking relatively high oral doses of this compound are very low, typically in the nanomolar range (reviewed in Ref. 4). For instance, a recent study examined the pharmacokinetics of a curcumin preparation in 12 healthy human volunteers 0.25-72 hr after an oral dose of 10 or 12 g. Using a high-performance liquid chromatography assay with a limit of detection of 50 ng mL À1 , only 1 subject had detectable free curcumin at any of the time points assayed. 5 The fact that curcumin also undergoes extensive metabolism in intestine and liver 6,7 means that high concentrations of curcumin cannot be achieved and maintained in plasma and tissues after oral ingestion. This is a major obstacle for the clinical development of this agent and suggests that the therapeutic potential of oral curcumin is limited. The low clinical efficiency of curcumin in the treatment of several chronic diseases such as Alzheimer's disease and cardiovascular diseases has been discussed recently. 8 As far as cancer is concerned, in vitro studies have demonstrated that cancer cells do not die unless they are exposed to curcumin concentrations of 5-50 lM for several hours. 4,9,10 Because of its poor bioavailability, these concentrations are not achieved outside the gastrointestinal tract when curcumin is taken orally. Because of its extensive metabolism in intestine and liver, these concentrations cannot be maintained for several hours in the gastrointestinal tract. This suggests that the chemotherapeutic potential of oral curcumin is limited even for the treatment of cancers of the gastrointestinal tract. Accordingly, when 15 patients with advanced colorectal cancer were treated with curcumin at daily doses of 3.6 g for up to 4 months, no partial responses to treatment or decreases in tu...

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“…Moreover, the damage of lysosomal and mitochondrial by hydrogen peroxide was also prevented by 6-gingerol. By contrast, there is an increasing body of evidence to suggest the prooxidative effects of phytochemicals (Kelly et al, 2001;Cao et al, 2006). In our previous study, 6-gingerol can apparently act as a prooxidant.…”

Section: Rosmentioning

confidence: 63%

6-Gingerol Attenuates Hydrogen Peroxide-induced DNA Damage in Human Umbilical Vein Endothelia Cells

Wang

Yang

Jiang

et al. 2014

FSTR

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An imbalance of oxidation and antioxidation is one of the primary causes of atherosclerosis. The use of naturalplant compounds with effects has been proven to have clinical relevance. 6-Gingerol, one of the major components of ginger, has diverse pharmacologic effects. In this study, the chemoprotective effect of 6-gingerol against hydrogen peroxide-induced DNA damage in human umbilical vein endothelia cells (HUVECs) was investigated. The comet assay was used to monitor DNA strand breaks. To further elucidate the underlying mechanisms, we tested lysosomal membrane stability, mitochondrial membrane potential, the intracellular generation of reactive oxygen species (ROS) and reduced glutathione (GSH). Our data revealed that 6-gingerol significantly reduced the DNA strand breaks caused by hydrogen peroxide. 6-Gingerol effectively suppressed hydrogen peroxide-induced intracellular ROS formation. The GSH depletion in HUVECs was also attenuated by 6-gingerol pretreatment. Moreover, lysosomal membrane stability was destroyed and mitochondrial membrane potential decreased after treated by hydrogen peroxide. Those effects can be protected by 6-gingerol. These firmly indicate 6-gingerol has a strong protective ability against the DNA damage caused by hydrogen peroxide in HUVECs, and the mechanism may relate to the antioxidant activity. Our data suggest 6-gingerol may be beneficial in the prevention of atherosclerosis.

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Mitochondrial and Nuclear DNA Damage Induced by Curcumin in Human Hepatoma G2 Cells

Cited by 203 publications

References 33 publications

Carboplatin resistant human laryngeal carcinoma cells are cross resistant to curcumin due to reduced curcumin accumulation

Carboplatin resistant human laryngeal carcinoma cells are cross resistant to curcumin due to reduced curcumin accumulation

The dark side of curcumin

6-Gingerol Attenuates Hydrogen Peroxide-induced DNA Damage in Human Umbilical Vein Endothelia Cells

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