Chemoprotective effects of anthocyanin found in berries

Anthocyanins have been shown to exhibit anticarcinogenic activity against multiple cancer cell types in vitro, and the mechanism of action seems to be rather complex. Interest in the health benefits of these compounds derives from finding of their potent antioxidant capacity.

Many studies have tried to determine the contribution of berry anthocyanins to the reduced incidence of chronic diseases associated with fruit and vegetable consumption. However, there have been multiple mechanisms of action proposed for anthocyanin compounds, and it is likely that more than one mechanism is taking place at a time.

Antioxidative activity of berries

Oxidative stress induced by free radicals causes DNA damage, including base mutation, single- and double-strand breaks, DNA cross-linking, chromosomal breakage and rearrangement. Those oxidative modifications at oncogenes, tumor-suppressing genes and DNA-repair genes may lead to carcinogenesis.

The phenolic structure of anthocyanins is responsible for their high antioxidant activity as scavengers of reactive oxygen species (ROS), metal chelators and protein binders. Berry extracts or juices have been shown to exhibit high antioxidant capacity in numerous studies. In cell culture systems, berry anthocyanin extracts as well as pure anthocyanins have shown antioxidant activities on colon, intestinal, endothelial, liver, lung, breast, leukemic, and brain cells.

The reported mechanisms for those cell culture systems could be categorized as directly scavenging ROS, increasing the oxygen absorbing capacity of cells, stimulating activation of phase II enzymes through antioxidant response element pathway, developing anthocyanin-DNA copigmentation complex possible against oxidative damage of DNA, reducing the formation of DNA adducts, and chelating metals and binding proteins.

On the contrary, anthocyanidins produced ROS, showing pro-oxidant activities, as apoptosis inducers in HL-60 cells instead of the antioxidant activities of anthocyanidins in the inhibition of TPAinduced cell transformation in mouse skin JB6 cells. In later studies, anthocyanins were found to induce apoptosis through reactive oxygen species-mediated mitochondrial pathway.

Detoxification Activity

Carcinogens are activated by phase I enzymes and inactivated by phase II enzymes through a process called detoxification. The products from a typical phase I reaction are usually more reactive molecules than the parent molecules. If these reactive molecules are not further metabolized by phase II enzymes, they may react with DNA and develop DNA adducts, inducing carcinogenesis. Phase II enzymes include glutathione-S-transferases, UDP-glucuronosyl-transferase, Quinone reductase and others.

Concord grape juice, rich in anthocyanins, significantly inhibited in vivo mammary DMBA-DNA adduct formation by 34 and 56%, partially explained by highly increased liver activity of the phase II metabolizing enzyme. Treatment of anthocyanins on rat liver Clone 9 cells demonstrated positive effects on elevating the antioxidant capacity by activating expression of phase II enzymes (glutathione reductase, glutathione peroxidase, and glutathione S-transferase) and promoting activity of NAD(P)H: quinone oxidoreductase.

Therefore, it was concluded that the molecular mechanism was associated with the activation of antioxidant response elements upstream of genes that regulate the expression of phase II detoxification enzymes. However, the crude extracts, anthocyanin and proanthocyanidin fractions of four Vaccinium species (lowbush blueberry, bilberry, cranberry, and lingonberry) were not found to be highly active to induce quinone reductase (QR) that belongs to phase II detoxification enzymes while the ethyl acetate extracts were active QR inducers in vitro.

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