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Ellagic Acid

Ellagic acid is a polyphenol found in numerous plant foods. Strawberries, raspberries, pecans, walnuts, pomegranates, and Terminalia chebula are all sources of this anti-oxidant. Extracts from these plants are known to have the highest levels of Ellagic acid.

This compound is found in plants in the form of ellagitannins. These compounds form when polymers of gallic acid and hexahydroxydipenoyl (HHDP) become linked to glucose centers. HHDP is formed when two gallic acid groups bind side-by-side within a tannin molecule. Ellagic acid results when HHDP is cleaved from the tannin and spontaneously rearranges. Once ellagic acid

is in its active form, it is able to perform its many functions. Currently, ellagic acid is being studied for its anti-cancer and anti-carcinogenic properties. However, it was originally used for its ability to assist in the formation of blood clots (Bock P, 1981). It seems that ellagic acid has very promising characteristics that make it a perfect supplement to help maintain healthy cardiovascular function and cell growth.

Ellagic acid's anti-cancer properties seem to go beyond its anti-oxidant activity. As a scavenger, ellagic acid binds to free radicals, inactivating them and preventing their degenerative damage (Festa, 2001). In recent studies, ellagic acid has shown to also promote healthy cell growth and death. Healthy cells have a normal life span of approximately 120 days. This process is call apoptosis. Cancer cells do not undergo apoptosis, instead they multiply exponentially until they form a tumor and damage tissues and other cells in the body. More than 600 studies have been performed to test the anti-carcinogenic capability of ellagic acid. Some experiments have suggested that ellagic acid can be used to eliminate the mutated growth cycle of cancer cells. Perhaps the most notable study took place at the Hollings Institute of Cancer at the Medical University of South Carolina. According to Narayanan et al (1999) clinical tests have shown that cervical cancer cells experienced apoptosis within 72 hours when exposed to ellagic acid. It was reported that ellagic acid causes G1 arrest within 48hours of exposure in breast, pancreas, esophagus, skin, colon, and prostate cancer cells. Recent studies have suggested that

ellagic acid also increases the expression of the P53 gene, the main gene needed to arrest mutagenic activity (Li et al, 2005). The P53 gene is usually destroyed by cancer cells, allowing cancer growth to proceed unhindered. The P53 gene is activated when the body is under stress (DNA damage, hypoxia, viral infection). It is responsible for arresting cell division in order to allow DNA to stabilize and repair

itself (Velculescu, 1996). Preventing its degradation in cancer cells is a major step forward in cancer research.

According to RW Teel (1986) the mechanism of this anti-carcinogenic activity is believed to be found in the bonding ability of ellagic acid. Scientists have found that this compound can bind to DNA and mask the sites for mutagen and carcinogen binding in the lab. The geometric symmetry of the molecule allows it to link with the double helix in a manner that seems to occupy DNA sequences that would otherwise serve as active sites for mutagens and carcinogens (Teel, 1986).

Ellagic acids contain other properties that can aid in a number of bodily functions. Previous studies have shown that it possesses the ability to activate the Hageman factor. The Hageman factor (Factor XII) is a plasma protein or glycoprotein that is needed for blood clotting. Its activation helps to prevent hemorrhage (Ratnoff and Crum, 1964). Ellagic acid's anti-oxidant activities also allow it to further improve blood maintenance by helping to avoid coronary heart disease. According to Diaz M. et al (1997) a lower incidence of coronary heart disease is found in subjects that consumed dietary or supplemental anti-oxidants. Ellagic acid's activities in blood health and in cancer research make it an exceedingly beneficial supplement with limitless possibilities.

References

Bock P., Srinivasan K, Shore J. (1981). Activation of Intrinsic Blood Coagulation by Ellagic Acid: Insoluble Ellagic Acid-Metal complexes are activating species. Biochemistry. 20, 7258-7266.

Diaz M, Frei B, Vita J, Keaney J. (1997). Antioxidants and Atherosclerotic Heart Disease. New England Journal of Medicine. 337:408-416.

Festa F, Aglitti T, Duranti G, Ricordy R, Perticone P, Cozzi R. (2001). Strong antioxidant activity of ellagic acid in mammalian cells in vitro revealed by the comet assay. Anticancer Res. 21(6A):3903-8.

Li TM, Chen GW, Su CC, Lin JG, Yeh CC, Cheng KC, Chung JG. (2005). Ellagic acid induced p53/p21 expression, G1 arrest and apoptosis in human bladder cancer T24 cells. Anticancer Res. 25(2A):971-9

Narayanan B, Geoffrey O, Willingham MC, Re GG, Nixon DW. (1999). P53/P21 (WAF1/CIP1) expression an its possible role in G1 arrest and apoptosis in ellagic acid treated cancer. Cancer Lett. 136(2):215-21.

Ratnoff OD, Crum JD. (1964). Activation of the Hageman Factor By Solutions of Ellagic Acid. J Lab Clin Med. 63:359-377.

Teel RW. (1986). Ellagic Acid binding to DNA as a possible mechanism for its antimutagenic and anticarcinogenic action. Cancer Lett. 30(3):329-36.

Velculescu VE and El-Diery WS. (1996). Biological and clinical importance of the p53 tumor suppressor gene. Clinical Chemistry. 42:858-868.

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