Genetic and Carcinogenic Effects of Plant Flavonoids: An Overview

MacGregor, James T.

doi:10.1007/978-1-4684-4790-3_23

Cited by 35 publications

(22 citation statements)

References 63 publications

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“…Our findings may partially explain the contradicting evidence from experiments on dietary quercetin [43,91]. In certain cases quercetin aglycon could promote tumorigenesis and tumor growth [47] possibly by oxidative DNA damage in the presence of Cu 2+ [89]. We suggest that anticarcinogenic activity of quercetin aglycon is dose dependent and is influenced by the presence of cytotoxic agents as well as serum survival factors (cytokines, oxygen free radicals -OFR) [48,67].…”

Section: Discussionmentioning

confidence: 78%

Induction of apoptosis and NF-$\kappa$B by quercetin in growing murine L1210 lymphocytic leukaemic cells potentiated by TNF-$\alpha$

et al. 2000

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-Polyphenol quercetin induced apoptosis in proliferating murine L1210 lymphocytic cells. DNA damage, as well as apoptosis and withdrawal from the cell cycle were transient. The above mentioned death promoting activity of quercetin was enhanced by physiological concentrations of TNF-α. At the same time, indices of cell viability dropped. However, the extent and tendency of the initially enhanced cell mortality steadily diminished throughout the experiment. After 12 h the G2/M phase reappeared. After 24 h all indices almost returned to control levels indicating either the selection of subpopulation of unaffected leukaemic cells or cells developing resistance to the treatment. A DNA ladder of oligonucleosomes was observed for apoptogenic treatments. We conclude that quercetin unmasked cell death, promoting the activity of TNF-α. However, after 12 and 24 h of exposure, surviving cells could complete the cell cycle and finally recover. At the same time, increased NF-κB activation was demonstrated by immunoblotting of the immunoreactive RelA/p65 subunit in nuclear extracts. Exposure to TNF-α or quercetin was crucial for increased activity of NF-κB, which may implicate an increasing resistance to their cytotoxicity. quercetin / TNF-α / leukaemia / apoptosis / NF-κB Reprod. Nutr. Dev. 40 (2000) 441

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Section: Discussionmentioning

confidence: 78%

Induction of apoptosis and NF-$\kappa$B by quercetin in growing murine L1210 lymphocytic leukaemic cells potentiated by TNF-$\alpha$

et al. 2000

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“…We also previously reported that apigenin induces cell cycle arrest (11) and p21/WAF1 upregulation in a tumor suppressor p53-independent manner (12). Moreover, although some flavonoids are mutagenic (13), apigenin has no mutagenic activity (14). Thus, apigenin is a promising and safe antitumor agent.…”

Section: Introductionmentioning

confidence: 82%

The dietary flavonoid apigenin sensitizes malignant tumor cells to tumor necrosis factor–related apoptosis-inducing ligand

Horinaka

Yoshida

Shiraishi

et al. 2006

Molecular Cancer Therapeutics

118

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Dietary flavonoid apigenin is expected to have preventive and therapeutic potential against malignant tumors. In this report, we show for the first time that apigenin markedly induces the expression of death receptor 5 (DR5) and synergistically acts with exogenous soluble recombinant human tumor necrosis factor -related apoptosis-inducing ligand (TRAIL) to induce apoptosis in malignant tumor cells. TRAIL is a promising candidate for cancer therapeutics due to its ability to selectively induce apoptosis in cancer cells. The combined use of apigenin and TRAIL at suboptimal concentrations induces Bcl-2-interacting domain cleavage and the activation of caspases-8, -10, -9, and -3. Furthermore, human recombinant DR5/Fc chimera protein and caspase inhibitors dramatically inhibit apoptosis induced by the combination of apigenin and TRAIL. On the other hand, apigenin-mediated induction of DR5 expression is not observed in normal human peripheral blood mononuclear cells. Moreover, apigenin does not sensitize normal human peripheral blood mononuclear cells to TRAIL-induced apoptosis. These results suggest that this combined treatment with apigenin and TRAIL might be promising as a new therapy against malignant tumors. [Mol Cancer Ther 2006;5(4):945 -51]

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“…According to MacGregor (1986), quercetin causes frameshift and base substitution mutations, and Gaspar et al (1993) consider it responsible for the mutagenic activity of red wine. This activity said to derive from the generation of reactive oxygen species (ROS) by autooxidation.…”

Section: Discussionmentioning

confidence: 99%

Mutagenicity of two species of the genus Alchornea measured by Salmonella microsome assay and micronucleus test

Santos¹,

Calvo²,

Cólus³

et al. 2010

Rev. bras. farmacogn.

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Some species of the plant genus Alchornea (family Euphorbiaceae) are widely used in popular medicine, mainly in South America and in Africa. Several kinds of biological activity have been seen in the species: antioxidant, antifungal, anti-inflammatory, antibacterial, cytotoxic against tumor cell lines and inhibitory to the replication of HIV-1 and HIV-2. In Brazil, the species Alchornea castaneaefolia Willd. A. Juss. and Alchornea glandulosa Poepp. & Endl. are used by the local population to treat rheumatism, arthritis and muscular pains. In view of the popular use of these plants as medicines and the potential risks from their consumption, we assessed the mutagenic potential of chloroform and methanol extracts of the leaves of these plant species, employing the in vivo micronucleus test and the Ames assay. The data obtained showed that the chloroform extracts were not mutagenic. The methanol extract of A. castaneaefolia was mutagenic to strain TA98 of Salmonella typhimurium and the methanol extract of A. glandulosa to strains TA98 and TA97a. The methanol extracts of both species of Alchornea were mutagenic in vivo at the largest dose employed. The probable mutagenic agents involved were the aglycone quercetin and amentoflavone, present in both species.

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Genetic and Carcinogenic Effects of Plant Flavonoids: An Overview

Cited by 35 publications

References 63 publications

Induction of apoptosis and NF-$\kappa$B by quercetin in growing murine L1210 lymphocytic leukaemic cells potentiated by TNF-$\alpha$

Induction of apoptosis and NF-$\kappa$B by quercetin in growing murine L1210 lymphocytic leukaemic cells potentiated by TNF-$\alpha$

The dietary flavonoid apigenin sensitizes malignant tumor cells to tumor necrosis factor–related apoptosis-inducing ligand

Mutagenicity of two species of the genus Alchornea measured by Salmonella microsome assay and micronucleus test

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