Chemopreventive potential of dietary bioflavonoids against 20-methylcholanthrene-induced tumorigenesis

Vellaichamy, Elangovan; Sekar, N.; Govindasamy, S.

doi:10.1016/0304-3835(94)90416-2

Cited by 160 publications

(77 citation statements)

References 15 publications

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“…This observation is in agreement with potentiating antitumour effects of a few flavonoids observed in vitro (Elangovan et al, 1994;Sliutz et al, 1996;Debes et al, 2003). The background for this effect may be that the concentration of GSH may play a role in STS chemoresistance (Hochwald et al, 1997) and that GSH depletion may increase the antitumour efficacy (Siemann and Beyers, 1997).…”

Section: Discussionsupporting

confidence: 88%

The effect of monohydroxyethylrutoside on doxorubicin-induced cardiotoxicity in patients treated for metastatic cancer in a phase II study

et al. 2007

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The purpose of this study was to investigate the cardioprotective effect of the semisynthetic flavonoid 7-monohydroxyethylrutoside (monoHER) on doxorubicin (DOX)-induced cardiotoxicity in a phase II study in patients with metastatic cancer. Eight patients with metastatic cancer were treated with DOX preceded by a 10 min i.v. infusion of 1500 mg m À2 monoHER. Five patients were examined by endomyocardial biopsy after reaching a cumulative dose of 300 mg m À2 . Histopathological changes in the cardiomyocytes (Billingham score) were compared with those described in literature for patients treated with DOX only. The mean biopsy score of the patients was higher (2.7) than the mean score (1.4) of historical data of patients who received similar cumulative doses of DOX. Although there is a considerable variability in few investigated patients, it was indicative that monoHER enhanced DOX-induced cardiotoxicity. However, the antitumour activity of DOX seemed better than expected: three of the four patients with metastatic soft-tissue sarcoma had a partial remission and the fourth patient stable disease. It is likely that the relatively high dose of monoHER is responsible for the lack of cardioprotection and for the high response rate in patients with soft-tissue sarcoma possibly by depleting the glutathione defense system in both heart and tumour.

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Section: Discussionsupporting

confidence: 88%

The effect of monohydroxyethylrutoside on doxorubicin-induced cardiotoxicity in patients treated for metastatic cancer in a phase II study

et al. 2007

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“…Some studies also reported that DR5 is more strongly expressed in cancer cells than in normal cells (Ichikawa et al, 2001;Koornstra et al, 2003). Previous studies in vivo have shown the biological effects of luteolin, such as preventing carcinogenesis in mice (Elangovan et al, 1994;Ueda et al, 2003). When rats were orally given luteolin, the total luteolin concentration was 15.5 mM in the blood plasma 30 min after dosing (Shimoi et al, 1998).…”

Section: Discussionmentioning

confidence: 98%

“…The cancer preventing effect of luteolin has been examined in terms of the incidence of fibrosarcoma induced by a mutagen in mice, and was found to bring about a significant reduction in the incidence of tumors and death of mice fed luteolin-mixed diets (Elangovan et al, 1994). A potent preventive effect via topical application of luteolin was also observed for the antitumor promotion of skin papillomas in mice (Ueda et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Luteolin induces apoptosis via death receptor 5 upregulation in human malignant tumor cells

et al. 2005

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Luteolin, a naturally occurring flavonoid, induces apoptosis in various cancer cells. Little is known however concerning the underlying molecular mechanisms responsible for this activity. In this report, we reveal a novel mechanism by which luteolin-induced apoptosis occurs, and show for the first time that the apoptosis by luteolin is mediated through death receptor 5 (DR5) upregulation. Luteolin markedly induced the expression of DR5, along with Bcl-2-interacting domain cleavage and the activation of caspase-8, -10, -9 and -3. In addition, suppression of DR5 expression with siRNA efficiently reduced luteolininduced caspase activation and apoptosis. Human recombinant DR5/Fc also inhibited luteolin-induced apoptosis. On the other hand, luteolin induced neither DR5 protein expression nor apoptosis in normal human peripheral blood mononuclear cells. These results suggest that DR5 induced by luteolin plays a role in luteolin-induced apoptosis, and raises the possibility that treatment with luteolin might be promising as a new therapy against cancer.

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“…For example, quercetin administered to rats in combination with dimethylbenz[a]anthracene (DMBA) or N-nitrosomethylurea (NMU) reduces the incidence and multiplicity of mammary tumours by 30 and 50 % respectively (Verma et al 1988). Quercetin and luteolin (10 g=kg diet) decrease ®brosarcoma incidence (52 % and 60 % respectively) and tumour size in male Swiss albino mice following treatment with the model chemical carcinogen 20-methylcholanthrene (Elangovan et al 1994). Quercetin (20 g=kg) also increases the survival and reduces the tumour burden of mice (Balb=c) transplanted intrasplenically with ML-3 hepatoma cells (Chi et al 1997).…”

Section: Animal Modelsmentioning

confidence: 99%

Plant polyphenols in cancer and heart disease: implications as nutritional antioxidants

Duthie¹,

Duthie²,

Kyle³

2000

Nutr. Res. Rev.

678

404

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Certain dietary antioxidants such as vitamin E and vitamin C are important for maintaining optimum health. There is now much interest in polyphenolic products of the plant phenylpropanoid pathway as they have considerable antioxidant activity in vitro and are ubiquitous in our diet. Rich sources include tea, wine, fruits and vegetables although levels are affected by species, light, degree of ripeness, processing and storage. This confounds the formulation of databases for the estimation of dietary intakes. Most attention to date has focused on the¯avonoids, a generic term which includes chalcones,¯avones,¯avanones,¯avanols and anthocyanins. There is little convincing epidemiological evidence that intakes of polyphenols are inversely related to the incidence of cancer whereas a number of studies suggest that high intakes of¯avonoids may be protective against CHD. In contrast, numerous cell culture and animal models indicate potent anticarcinogenic activity by certain polyphenols mediated through a range of mechanisms including antioxidant activity,

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Chemopreventive potential of dietary bioflavonoids against 20-methylcholanthrene-induced tumorigenesis

Cited by 160 publications

References 15 publications

The effect of monohydroxyethylrutoside on doxorubicin-induced cardiotoxicity in patients treated for metastatic cancer in a phase II study

The effect of monohydroxyethylrutoside on doxorubicin-induced cardiotoxicity in patients treated for metastatic cancer in a phase II study

Luteolin induces apoptosis via death receptor 5 upregulation in human malignant tumor cells

Plant polyphenols in cancer and heart disease: implications as nutritional antioxidants

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