New Study Reveals Lycopene From Tomatoes May Activate Special Cancer Preventive Enzymes

The good news keeps coming about the cancer preventive effect of tomatoes and tomato products. The results of a new study will be released during the American Association for Cancer Research (AACR) annual meeting (March 27-31), that suggests that a diet rich in tomato products may activate special cancer-preventive enzymes called "phase II" detoxification enzymes. These enzymes effectively remove harmful carcinogens from the cells and from the body.

It has long been thought that the carotenoids found in fruits and vegetables have a cancer preventive effect. In particular, epidemiological studies have found that as the consumption of tomato products increases, risk of certain types of cancer decreases.

The new research suggests that consumption of carotenoid-rich tomato products may exert their cancer-preventive effect by stimulating the body's "antioxidant response element" (ARE). When Dr. Joseph Levy and his colleagues at Ben-Gurion University of the Negev, Beer-Sheva, Israel, incubated breast and liver cancer cells with lycopene, the level of phase II detoxification enzymes increased. (Beta carotene and another tomato carotenoid called phytoene had a lesser effect).1

Their results suggest that activation of the ARE-driven induction of phase II enzymes by lycopene represents a unique mechanism for the cancer-preventive action of a diet rich in tomato products.

"The results suggest that a diet rich in tomato products may help trigger a unique cancer preventive mechanism," said Dr. Levy.

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1. Carotenoids activate the antioxidant response element (ARE) transcription system Joseph Levy, Anat Ben-Dor, Noga Dubi, Michael Danilenko, Anat Zick, Yoav Sharoni. Ben-Gurion University of the Negev, Beer-Sheva, Israel

Epidemiological studies have found an inverse association between the consumption of tomato products and the risk of certain types of cancers. Induction of phase II detoxification enzymes seems to be an important mechanism by which phytonutrients prevent cancer. Expression of phase II enzymes, such as NAD(P)H:quinone oxidoreductase (NQO1) and ?-glutamylcysteine synthetase (GCS), is regulated by the antioxidant response element (ARE), which is found in the promoters of genes encoding these proteins. The nuclear transcription factor Nrf2 binds to the ARE and positively regulates the expression of phase II enzymes. We tested whether carotenoids exert their cancer-preventive effect by stimulation of ARE and induction of NQO1 and GCS. In transiently transfected MCF-7 mammary cancer cells and HepG2 hepatoma cells, lycopene transactivated the expression of a reporter gene (luciferase) fused with ARE sequences.

The transactivation was dose-dependent and unexpectedly specific for lycopene, since astaxanthin, ß-carotene and phytoene had no effect. This specificity suggests that activation of ARE-mediated transcription by carotenoids is not related solely to their antioxidant properties. Measurement of carotenoid-induced changes in the intracellular levels of reactive oxygen species using a fluorescent probe (dichlorofluorescein diacetate) further supported this conclusion. In accordance with the transactivation data, lycopene treatment caused an increase in NQO1 and GCS protein levels in both MCF-7 and HepG2 cells.

A lower potency was found for ß-carotene, whereas astaxanthin and phytoene had no effect whatsoever. The induction of GCS protein was accompanied by an increase in the cellular levels of glutathione, a potent substrate for carcinogen detoxification. Nrf2 was found predominantly in the cytoplasm in non-treated (control) cells, but appeared predominantly in the nucleus after treatment with both tert-butylhydroquinone (the known ARE activator) and lycopene. Other carotenoids also induced Nrf2 translocation but with a lower potency.

Our results suggest that activation of the ARE-driven induction of phase II enzymes by lycopene represents a novel molecular mechanism for the cancer-preventive action of a diet rich in tomato products.

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